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Current Clinical Urology
Eric A. Klein, MD, Series Editor

For further volumes:


Cancer and Sexual Health


John P. Mulhall, MD
Department of Surgery, Memorial Sloan-Kettering
Cancer Center, New York, NY, USA

Associate Editors

Luca Incrocci, MD
Department of Radiation Oncology, Erasmus MC-Daniel den
Hoed Cancer Center, Rotterdam, The Netherlands
Irwin Goldstein, MD
Director, Sexual Medicine, Alvarado Hospital,
San Diego, CA, USA
Clinical Professor of Surgery, University of California
at San Diego, San Diego, CA, USA
Raymond C. Rosen, PhD
New England Research Institutes, Watertown, MA, USA

John P. Mulhall, MD Irwin Goldstein, MD
Department of Surgery Director Sexual Medicine
Memorial Sloan-Kettering Alvarado Hospital
Cancer Center San Diego, CA
New York, NY USA
USA and Clinical Professor of Surgery
University of California at San Diego
Luca Incrocci, MD San Diego, CA
Department of Radiation Oncology USA
Erasmus MC-Daniel den
Hoed Cancer Center
Rotterdam Raymond C. Rosen, PhD
The Netherlands New England Research Institutes Watertown, MA

ISBN 978-1-60761-915-4 e-ISBN 978-1-60761-916-1
DOI 10.1007/978-1-60761-916-1
Springer New York Dordrecht Heidelberg London

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Due to the nature of my practice in my capacity as the Director of Male
Sexual & Reproductive Medicine at Memorial Sloan-Kettering Cancer
Center, it has become clear to me that to date there does not exist a reference
work devoted to the link between cancer and human sexuality. Thus, it has
been an ambition of mine for some time to develop this book. The purpose
of this text is to act as a resource for those clinicians caring for cancer
patients as well as act as a reference text for the sexual medicine clinician
who may not see a large number of cancer patients. I hope that physicians,
researchers, nurses, and clinician trainees will find this a valuable resource.
In the twenty-first century, while cancer is endemic, so too is the survival
of the cancer patient. It is well recognized that the diagnosis of cancer rep-
resents a major stressor in a person’s life. Add to this the common treat-
ments for cancer and one can see the potential for a negative effect of cancer
on a person’s sexual health. Increasingly, patients are winning their battle
with cancer and are surviving long periods of time. We see daily in practice
patients with cancer of the testis, prostate, breast colon, and hematologic
malignancies. So, the concept of survivorship has become increasingly
important to cancer clinicians. Survivorship has become a medical specialty
itself and refers to the focus not just on curing cancer, but also dealing with
the consequences of the diagnosis and treatment of that cancer. It has been
recognized that for many cancer survivors, sexual function represents a sig-
nificant concern. I hope this book will help you in the management of the
survivorship issues of your patients.
Such an opus is impossible to accomplish without the assistance of many
different parties. First of all, I would like to thank the associate editors of
this project who were integral to the development of the table of contents,
the selection of the authors, and finally the review of the manuscripts. In the
world of sexual medicine, all three are instantly recognizable names. Dr. Irwin
Goldstein is a urologist and one of the founding fathers of modern sexual
medicine. He has been a mentor to me since my training with him 15 years
ago and is the current editor-in-chief of the Journal of Sexual Medicine.
Dr. Raymond Rosen is an eminent clinician-scientist who has spent three
decades treating patients with sexual problems, researching sexual prob-
lems, and educating future sexual medicine clinicians. He is the lead scien-
tist at the New England Research Institute, one of the preeminent


vi Preface

epidemiologic research centers in the United States. Dr. Luca Incrocci is a
radiation oncologist, an executive board member of the International Society
for Sexual Medicine, and the world’s foremost authority on the impact of
radiation on sexual function. I would like to thank each and every one of the
authors who have contributed to this book. For anyone who has written a
book chapter, it is easy to understand how much work this entails. I believe
we have congregated the world’s leading experts in their respective areas.
Finally, I would like to extend my sincerest gratitude to the staff at
Springer for the expert guidance and assistance in bringing this idea from
the initial vision to the completed work. A debt of gratitude is due to Paul
Dolgert for spearheading the initial effort which was expertly taken over by
Richard Hruska for the completion of the project. Finally, to Kathryn Hiler
for practicing the proverbial “herding of cats” in getting all of the manu-
scripts into production.
I hope this book will be a success, will help you in your daily practice,
and will translate into helping our cancer patients. In the 12 months or so
since this project started, we as editors already have ideas about chapters
that are missing and topics not covered, which we will hopefully address in
the next volume of this work.
New York, NY John P. Mulhall, MD


Part I  Normal Sexual Function

  1 Functional Anatomy of the Male Sex Organs.......................... 3
Anthony J. Bella and Rany Shamloul

  2 Functional Anatomy of the Female Sex Organs....................... 13
Van Anh T. Ginger and Claire C. Yang

  3 Physiology of Libido................................................................... 25
James G. Pfaus

  4 Physiology of Orgasm................................................................. 35
Roy J. Levin

  5 Physiology of Female Genital Sexual Arousal.......................... 51
Irwin Goldstein and Jonathan Silberstein

  6 Physiology of Erection................................................................ 69
Alan W. Shindel and Tom F. Lue

  7 Physiology of Ejaculation........................................................... 77
Pierre Clément and François Giuliano

Part II  Disorders of Sexual Function

  8 Classifying Female Sexual Dysfunction.................................... 93
Annamaria Giraldi

  9 Hypoactive Sexual Desire Disorder........................................... 105
Alessandra H. Rellini, Melissa A. Farmer, and Gale H. Golden

10 Disorders of Female Sexual Arousal......................................... 125
Tuuli M. Kukkonen and Sabina Sarin

11 Disorders of Female Orgasm..................................................... 147
Yasisca P. Khouri, Corey Pallatto Hughan, and Cindy M. Meston


viii Contents

12 Sexual Pain Disorders................................................................. 163
Corrie Goldfinger and Caroline F. Pukall

13 Erectile Dysfunction: Prevalence and Pathophysiology.......... 183
Antonino Saccà and Francesco Montorsi

14 Androgen Deficiency................................................................... 195
Mathew C. Raynor, Michael R. Pinsky, Arthi Chawla,
and Wayne J.G. Hellstrom

15 Peyronie’s Disease....................................................................... 217
Frederick L. Taylor and Laurence A. Levine

16 Disorders of Ejaculation and Male Orgasm............................. 235
Chris G. McMahon

17 Priapism....................................................................................... 259
Trinity J. Bivalacqua, Helen R. Levey,
and Arthur L. Burnett

Part III  Patient Assessment

18 The Sexual Health Interview: Male........................................... 281
Kevan Wylie and Julie Fitter

19 The Sexual Health Interview: Female....................................... 291
Sharon J. Parish and Sheryl A. Kingsberg

20 Communication About Sexuality and Cancer.......................... 307
Susan Carr

21 Validated Questionnaires in Female Sexual
Function Assessment................................................................... 317
Tierney A. Lorenz, Kyle R. Stephenson,
and Cindy M. Meston

22 Validated Questionnaires in Male Sexual
Function Assessment................................................................... 339
Raymond C. Rosen and Christian J. Nelson

23 Evaluation of the Female with Sexual Dysfunction................. 351
Michael L. Krychman, Don Dizon, Alison Amsterdam,
and Susan Kellogg Spadt

24 Evaluation of Male Sexual Dysfunction.................................... 357
Gregory A. Broderick

Contents ix

25 The Impact of Cancer on the Partner’s Sexuality................... 383
Eusebio Rubio-Aurioles

26 Gay and Lesbian Patients with Cancer..................................... 397
Anne Katz

Part IV  Cancer and Sex

27 The Impact of a Cancer Diagnosis on Sexual Health.............. 407
Christian J. Nelson, Jason Gilley, and Andrew J. Roth

28 Breast Cancer.............................................................................. 415
Stacy Tessler Lindau, Stacey Sandbo, Shari Beth Goldfarb,
and Maura N. Dickler

29 Gynecological Cancers................................................................ 457
J. Bitzer and J. Alder

30 Pelvic Surgery for Urological Cancers...................................... 477
Nelson E. Bennett and John P. Mulhall

31 Pelvic Radiation in Men............................................................. 489
Luca Incrocci

32 Pelvic Radiation in Women........................................................ 503
Pernille T. Jensen

33 Impact of Chemotherapy and Hormone Therapy
on Female Sexual Health............................................................ 525
Rossella E. Nappi, Francesca Albani, Maria Rosa Strada,
and Emmanuele Jannini

34 Impact of Androgen Deprivation Therapy
on Men’s Sexual Health.............................................................. 535
Claudio A. Romero, Anthony N. Hoang, and Run Wang

35 Colorectal Cancer....................................................................... 549
Klaas Havenga, Stephanie O. Breukink,
and Marian J.E. Mourits

36 Stem Cell Transplant.................................................................. 561
Jean C. Yi and Karen L. Syrjala

37 Sexual Health in the Terminally Ill........................................... 577
W.L. Gianotten and J.A. Hordern

x Contents

Part V  Treatment Strategies

38 Survivorship: An Overview........................................................ 591
Mary S. McCabe and Joanne Kelvin

39 Nutriceuticals in Sexual Health................................................. 603
Mark A. Moyad

40 Medical Treatments for Sexual Problems in Women.............. 627
Alessandra Graziottin and Audrey Serafini

41 Surgical Treatments for Sexual Problems in Women.............. 643
Lara J. Burrows and Andrew T. Goldstein

42 Sex Therapy in Female Sexual Dysfunction............................. 649
Linda L. Banner

43 Erectile Function Preservation for Men with Cancer.............. 657
Raanan Tal and John P. Mulhall

44 Erectile Dysfunction: Pharmacological Therapy..................... 675
Tariq F. Al-Shaiji, Eric Chung, and Gerald B. Brock

45 Erectile Dysfunction: Devices.................................................... 697
Stephen E. McKim and Culley C. Carson III

46 The Management of Premature Ejaculation............................ 709
Marcel D. Waldinger

47 Testosterone Therapy in the Male Cancer Patient................... 721
Abraham Morgentaler

48 Sex Therapy in Male Sexual Dysfunction................................. 731
Stanley E. Althof and Rachel B. Needle

49 Restoring Intimacy in Relationships Affected by Cancer....... 739
Sharon Manne

50 Dating and Disclosure for Cancer Survivors............................ 751
Rachel Hamilton and Brad Zebrack

Index .................................................................................................... 763


Tierney A. Lorenz
Department of Psychology, University of Texas at Austin,
1 University Station A8000, Austin, TX 78712, USA
Francesca Albani
Gynecological Endocrinology and Menopause Unit,
Department of Internal Medicine and Endocrinology, IRCCS
Maugeri Foundation, University of Pavia, Pavia, Italy;
IRCCS Fondazione “S. Maugeri”, Via Ferrata 8, 27100, Pavia, Italy
Tariq F. Al-Shaiji
Divison of Urology, University of Western Ontario, London, ON, Canada
J. Alder
Division of Social Medicine and Psychosomatics,
Department of Obstetrics and Gynecology,
University Women’s Hospital Basel, Basel, Switzerland
Stanley E. Althof
University of Miami Miller School of Medicine, Miami, FL, USA;
Center for Marital and Sexual Health of South Florida,
West Palm Beach, FL 33401, USA
Alison Amsterdam
Mount Sinai School of Medicine, New York, NY, USA
Linda L. Banner
Center for Sexual Health, San Jose, CA 95124, USA
Anthony J. Bella
Greta and John Hansen Chair in Men’s Health Research,
Division of Urology, Department of Surgery, University of Ottawa,
Ottawa, ON, Canada
Nelson E. Bennett
Department of Surgery, Urology Service, Memorial Sloan-Kettering
Cancer Center, New York, NY, USA
J. Bitzer
University Women’s Hospital Basel, 4031 Basel, Switzerland


xii Contributors

Trinity J. Bivalacqua
The James Buchanan Brady Urological Institute, Johns Hopkins Hospital,
Baltimore, MD 21287, USA
Stephanie O. Breukink
Department of Surgery, University Hospital Maastricht, Groningen,
The Netherlands
Gerald B. Brock
Division of Urology, University of Western Ontario, London, ON, Canada
Gregory A. Broderick
Department of Urology, Mayo Clinic College of Medicine, Jacksonville,
FL 32224, USA
Arthur L. Burnett
The James Buchanan Brady Urological Institute, Johns Hopkins Hospital,
Baltimore, MD 21287, USA
Lara J. Burrows
Summa Health System, Akron, OH, USA
Susan Carr
Head of Psychosexual Service, Royal Womens Hospital, Parkville,
VIC, Australia
Culley C. Carson, III
Division of Urology, University of North Carolina, Chapel Hill, NC, USA
Arthi Chawla
Department of Urology, Section of Andrology, Tulane University Health
Sciences Center, New Orleans, LA 70112, USA
Eric Chung
Department of Urology, Princess Alexandra Hospital, Ipswich Rd,
Woolloongabba, QLD 4103, Australia
Pierre Clément
Pelvipharm Laboratories, Orsay, France
Maura N. Dickler
Department of Medicine, Memorial Sloan-Kettering Cancer Center,
New York, NY, USA
Don S. Dizon
Obstetrics-Gynecology and Medicine, The Warren Alpert Medical
School of Brown University, Providence, RI, USA
Melissa A. Farmer
Department of Psychology, McGill University, Montreal, QC, Canada
Julie Fitter
Department of Sexual Medicine, Porterbrook Clinic,
Sheffield S11 9BF, UK

Contributors xiii

W.L. Gianotten
Rehabilitation Sexology, Centre for Physical Rehabilitation,
De Trappenberg, Huizen, The Netherlands
Jason Gilley
Van Anh T. Ginger
Department of Urology, University of Washington, Harborview Medical
Center, Seattle, WA, USA
Annamaria Giraldi
Psychiatric Center Copenhagen, Sexological Clinic, Copenhagen, Denmark
François Giuliano
Pelvipharm laboratories, Orsay, France;
Department of Physical Medicine and Rehabilitation, Neuro-Uro-
Andrology Unit, Raymond Poincaré Hospital,, Garches, France;
EA4501, University of Versailles-St Quentin en Yvelines, Orsay, France
Gale H. Golden
Department of Psychiatry, Private Practice, University of Vermont
Medical College, Burlington, VT, USA
Shari Beth Goldfarb
Departments of Medicine and Epidemiology and Biostatistics,
Memorial Sloan-Kettering Cancer Center, New York, NY, USA
Corrie Goldfinger
Department of Psychology, Queen’s University, Kingston, ON, Canada
Andrew T. Goldstein
Department of Obstetrics and Gynecology, The George Washington
University School of Medicine, Washington, DC, USA
Irwin Goldstein
Sexual Medicine, Alvarado Hospital, San Diego, CA, USA;
University of California at San Diego, San Diego, CA, USA
Alessandra Graziottin
Center of Gynecology and Medical Sexology, H.San Raffaele Resnati,
Via Santa Croce 10/A, 20123 Milan, Italy
Rachel Hamilton
University of Michigan, School of Social Work, Ann Arbor, MI 48109, USA
Klaas Havenga
Department of Surgery, University Medical Center Groningen,
Groningen, The Netherlands
Wayne J.G. Hellstrom
Department of Urology, Section of Andrology, Tulane University Health
Sciences Center, New Orleans, LA 70112, USA
Anthony N. Hoang
Division of Urology, University of Texas Medical School at Houston,
Houston, TX 77030, USA

xiv Contributors

J.A. Hordern
Cancer Council Victoria, Cancer Information and Support Service,
1 Rathdowne Street, Carlton, 3053
Luca Incrocci
Department of Radiation Oncology, Daniel den Hoed Cancer Center,
Rotterdam, The Netherlands
Emmanuele Jannini
School of Sexology, University of L’Aquila, L’Aquila, Italy
Pernille T. Jensen
Subspecialist Consultant Gynaecologic Oncology, Department of
Gynecology and Obstetrics, Copenhagen University Hospital Herlev,
Herlev, Denmark
Anne Katz
Manitoba Prostate Center, Cancer Care Manitoba, Winnipeg, MB, Canada
Joanne Kelvin
Memorial Sloan-Kettering Cancer Center, New York, NY 10021, USA
Sheryl A. Kingsberg
Division of Behavioral Medicine, University Hospitals Case Medical
Center, Cleveland, OH, USA;
Department of Reproductive Biology and Psychiatry, Case Western
Reserve University, School of Medicine, Cleveland, OH, USA
Michael L. Krychman
Medical Director of Sexual Medicine Hoag Hospital, Executive Director
of the Southern California Center for Sexual Health and Survivorship
Medicine, Associate Clinical Attending University of Southern California,
Newport Beach, CA 92663, USA
Tuuli M. Kukkonen
Department of Family Relations and Applied Nutrition,
University of Guelph, 50 Stone Road East Guelph, ON, Canada
Helen R. Levey
The James Buchanan Brady Urological Institute, Johns Hopkins Hospital,
Baltimore, MD 21287, USA
Roy J. Levin
Sexual Physiology Laboratory, Porterbrook Clinic, Sheffield S11 9BF,
Yorkshire, England
Laurence A. Levine
Department of Urology, Rush University Medical Center, Chicago,
IL 60612, USA
Stacy Tessler Lindau
Department of Obstetrics and Gynecology, Department of Medicine-
Geriatrics, The University of Chicago, Chicago, IL 60637, USA

Contributors xv

Tom F. Lue
Department of Urology, University of California at San Francisco,
San Francisco, CA, USA
Sharon Manne
Section Chief of Population Studies, The Cancer Institute of New Jersey,
Professor of Medicine, UMDNJ – Robert Wood Johnson Medical School
Mary S. McCabe
Memorial Sloan-Kettering Cancer Center, New York, NY 10021, USA
Stephen E. McKim
Division of Urology, University of North Carolina, Chapel Hill, NC, USA
Chris G. McMahon
University of Sydney, Australian Center for Sexual Health, Sydney, Australia;
Berry Road Medical Center, Suite 2-4, 1a Berry Road, St Leonards,
NSW 2065, Australia
Cindy M. Meston
Department of Psychology, University of Texas at Austin, Austin,
TX 78712, USA
Francesco Montorsi
Department of Urology, Vita-Salute San Raffaele University, Milan, Italy
Abraham Morgentaler
Division of Urology, Beth Israel Deaconess Medical Center,
Harvard Medical School, Boston, MA 02445, USA
Marian J.E. Mourits
Department of Gynaecology, University Medical Center Groningen,
University of Groningen, Groningen, The Netherlands
Mark A. Moyad
Department of Urology, University of Michigan Medical Center,
Ann Arbor, MI 48109-0330, USA
John P. Mulhall
Department of Surgery, Urology Service, Memorial Sloan-Kettering
Cancer Center, New York, NY, USA
Rossella E. Nappi
Research Center for Reproductive Medicine, Section of Obstetrics
and Gynecology, Department of Morphological,
Eidological and Clinical Sciences, University of Pavia, Pavia, Italy;
Gynecological Endocrinology and Menopause Unit,
Department of Internal Medicine and Endocrinology,
IRCCS Maugeri Foundation, University of Pavia, Pavia, Italy;
IRCCS Fondazione “S. Maugeri”, Via Ferrata 8, 27100 Pavia, Italy
Rachel B. Needle
South University, Nova Southeastern University, Fort Lauderdale-Davie,
FL, USA; Positive Friends

New York. USA Caroline F. Penfield Avenue. USA Sharon J. Pukall Department of Psychology. Pallatto Department of Psychology. Canada Mathew C. Austin. Tulane University Health Sciences Center. Canada . Parish Department of Medicine. Section of Andrology. Romero Division of Urology. Austin. Bronx. Montreal. Watertown. Rosen New England Research Institutes. University of Texas Medical School at Houston. New Orleans. USA Eusebio Rubio-Aurioles Asociación Mexicana para la Salud Sexual.xvi Contributors Christian J. University of Texas at Austin. Albert Einstein College of Medicine and Montefiore Medical Center. McGill University. México Antonino Saccà Department of Urology. University of Vermont. Pfaus Department of Psychology. TX. ON. TX. University of Texas at Austin. NY 10022. USA Yasisca Pujols Department of Psychology. Center for Studies in Behavioral Neurobiology. 1205 Dr. QC. 20132 Milan. New Orleans. Montréal. A. LA 70112. Burlington. MA. Houston. USA Andrew J. Tezoquipa Mexico City. (AMSSAC). Nelson Department of Psychiatry and Behavioral Sciences. USA Raymond C. Canada Michael R. NY 10022. Vita-Salute San Raffaele University. Italy Stacey Sandbo Sabina Sarin Department of Psychology. TX 77030. USA Alessandra H. Section of Andrology. LA 70112. Rellini Department of Psychology. Memorial Sloan-Kettering Cancer Center. USA James G. USA Claudio A. Concordia University.C. Raynor Department of Urology. USA Corey A. Tulane University Health Sciences Center. Roth Department of Psychiatry and Behavioral Sciences. Kingston. Pinsky Department of Urology. QC. New York. Queen’s University. Memorial Sloan-Kettering Cancer Center. NY 10467. VT.

University of California at San Francisco. USA . Houston. USA. PA. CA. USA Maria Rosa Strada Rehabilitative Oncology Unit. Philadelphia. USA Frederick L. WA 98109.Contributors xvii Audrey Serafini Specialty School. Faculty of BetaSciences. San Raffaele Hospital. Taylor Department of Urology. The University of Texas MD Anderson Cancer Center at Houston. Pavia. University of Washington. Male Sexual and Reproductive Medicine Program. IRCCS. University of Utrecht. CA. University of Texas at Austin. Houston. Fred Hutchinson Cancer Research Center. Chicago. Shindel Department of Urology. WA 98109. Memorial Sloan-Kettering Cancer Center. TX 77030. Department of Surgery. Italy Rany Shamloul Division of Urology. Italy. Waldinger Division of Pharmacology. University of Ottawa. IRCCS Fondazione “S. University of California at San Diego. USA Raanan Tal Department of Surgery. Pavia. TX 78712. Maugeri Foundation. San Diego. ON. Ottawa. Seattle. Stephenson Department of Psychology. Via Ferrata 8. 3584 CG Utrecht. Rush University Medical Center. Clinical Research Division. Austin. USA. USA. Department of Urology. TX 77030. The Netherlands Run Wang Division of Urology. Milan. Department of Pharmaceutical Sciences. Fred Hutchinson Cancer Research Center. USA Kyle R. USA Susan Kellogg Spadt Pelvic and Sexual Health Institute of Philadelphia. Syrjala Biobehavioral Sciences. University of Texas Medical School at Houston. USA Marcel D. WA 98109. 27100. NY. USA Jonathan Silberstein Division of Urology. Maugeri”. Urology Service. Seattle. IL 60612. New York. Survivorship Program. Seattle. Italy Karen L. Universiteitsweg 99. Department of Psychiatry and Behavioral Sciences. San Francisco. Canada Alan W.

Fred Hutchinson Cancer Research Center. Seattle. WA. Yi Biobehavioral Sciences. Sheffield. Royal Hallamshire Hospital. Seattle. Harborview Medical Center.xviii Contributors Kevan Wylie Department of Sexual Medicine. UK. USA Brad Zebrack University of Michigan. Clinical Research Division. Sheffield. School of Social Work. USA . University of Washington. Department of Urology. WA 98109. Porterbrook Clinic. Ann Arbor. S11 9BF. MI 48109. USA Jean C. UK Claire C. Yang Department of Urology.

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Part I Normal Sexual Function .

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and allow the erect penis to achieve a University of Ottawa. Bella (*) Greta and John Hansen Chair in Men’s Health Research. epididymis. PhD Keywords  Anatomy • Prostate • Arterial supply of erectile tissue. There are two fascial corpus spongiosum. with at the coronal sulcus. Cancer and Sexual Health. The deeper fascial layer muscle allowing arterial blood to flow into the is Buck’s fascia.P. ON. LLC 2011 . On the other hand. including coverage of the deep dorsal vein as well as the dorsal neurovascular bundles.  1. © Springer Science+Business Media. The point at which the glans is Introduction draped over the penile shaft is known as the coro- nal sulcus. gives a reasonable including the penis as well as the testis. while the cor. Department of Surgery. Stretched penile The male genital system consists of both external length. fascia. ments attach to the pubic symphysis and Buck’s Division of Urology. as measured from the pubic junction to and internal sexual and reproductive organs. ernosa and the corpus spongiosum in separate pus spongiosum contains a considerable amount compartments. The folded portion is bilateral corpora cavernosa. It continues caudally as the organ (Fig. there it folds back on itself and attaches The penis is essentially a tripartite structure. an overview of the gross and micro- scopic anatomy of the male genitalia is provided. The length of the penis varies widely.).Chapter 1 Functional Anatomy of the Male Sex Organs Anthony J.1007/978-1-60761-916-1_1. Bella MD and Rany Shamloul MD. a midline ventral known as the prepuce. In this chapter.J. Dartos fascial layer of the scrotum and Colles’ tates an erection by complete relaxation of smooth fascia in the perineum. The corpora cavernosa facili. especially in the flaccid state. Ottawa. Mulhall et al. The fundiform and suspensory liga- A. the coronal sulcus or meatus. (eds. continuous with Scarpa’s fascia skin which can be moved freely over the erect of the abdomen. vas deferens. J. Skin and Fascia Penile skin is continuous with that of the lower Penis abdominal wall and continues over the glans penis. all three of which layers. which covers the corpora cav- corporal bodies. approximation of erect length [1]. the more superficial of which is the are surrounded by loose subcutaneous tissue and Dartos fascia. its main function is to provide • Cavernous nerves • Penis adequate covering to the male penile urethra and contributes little to erectile function. The glans (head) of the penis is an extension of the corpus spongiosum. seminal vesicle and the prostate.1). 3 DOI 10. Canada horizontal or upright angle. Current Clinical Urology. and glans.

Bella and R. In addition to providing a supportive frame- osal septum.2 mm at the 1 erectile bodies as well as functioning in the veno. which is akin to a midline strut. fibrillar collagen in orga. prostatectomy or with Peyronie’s disease may The composition and distribution of component compromise this function and lead to venous fibers is a fundamental factor in rendering the leak. Both fiber types are essential for as a backboard. Elastin content is also an important The tunica albigunea is a strong bilayered fibrous determinant of stretched penile length. The end-result is allows for tunical expansion as these fibers are maintenance of an erect penis. o’clock and 11 o’clock positions. The main function of this at the 5 o’clock and 7 o’clock positions (just lat- thick covering is to both provide rigidity of the eral to the corpus spongiosum) to 2. type I. and pierce the outer bundles in an oblique nized arrays throughout which are interspersed manner [5]. logical changes such as those seen postradical latticed network on which the collagen fibers rest. resulting in compression of the normal function: the steel-like tensile strength of emissary veins during penile engorgement and collagen is unyielding and resists uncontrolled limiting the amount of penile blood which is able deformity at high pressure.J. The corpus spongiosum lacks both the outer (struts) that traverse the cavernosal space and serve layer as well as the strong supports or struts. extrusion of longitudinally and the inner layer in a circular penile prosthesis is most common at this location fashion. the tunica albuginea tunica itself may be considered a “mesh” that is is essential to venous trapping and pathophysio- composed of elastic fibers that form an irregular. The inner layer contains strong supports [4]. the outer of which is oriented the ventral groove over the urethra. This coincides occlusive trapping mechanism. to expand the support provided by the intracavern. while elastin content to drain away from the corpora. sheath of heterogenous thickness that surrounds Thickness ranges from approximately 0. The work to the paired corpora. Inadequate venous .1  Cross-sectional anatomy of the penis Tunica Albigunea able to stretch to approximately 150% of “resting” length [3].8 mm the corpora cavernosa. The emissary veins travel between the inner function of the tunica. but also type III. Shamloul Fig.4 A. it is primarily composed of and outer layers of the tunica for short distances. The outer longitudinal layer serves elastin fibers [2]. 1. It is composed of with the absence of the outer longitudinal layer at two primary layers.

the engorged corpora cavernosa also contribute They are supported by several fibrous structures. two types of electrical areolar tissue [7. or traumatic denervation injury flaccid and erect states. responsible for changes in penile morphology in aging. may also cause loss of compliance [10]. it is still able The paired corpora cavernosa originate sepa. nosum: spontaneous and activity-induced [13]. fibroblasts. For example. the penile veins are externally compressed by the intracavernous struts radiating from the inner ischiocavernosus and bulbocavernosus muscles layer of tunica albuginea. further increasing terial fibrous sheaths. desmin or vimentin. (2) alteration in as a by-product of aging. resulting in and Spongiosum lesser venous occlusion [10]. 8]. trabeculae or endothelium. hypercho- smooth muscle. the glans penis. strength. and loose respectively [2]. The corpus spon. Cavernous albuginea. In the flaccid state. accounting for 45% of corporal volume [9]. With sexual penis are similar in internal structure to the stimulation and the release of neurotransmitters corpora cavernosa except that the sinusoids are (mainly nitric oxide – NO) from the cavernous larger and there is a lack of outer layer of tunica nerve terminals. Blood flow to the penis is giosum and its distal termination in the glans approximately 5 mL per minute [8]. or (5) congenital The structure of the corpus spongiosum is anomalous large venous channels [6]. The spongy inner portion engorgement and pressure in the glans and of the corpora consists mainly of interconnected spongiosum. to glanular tumescence. In humans. sinusoids separated by smooth muscle trabeculae. Intraspongiosal pressures reach only one-half to one-third that of the cavernosa due Corpora Cavernosa to the less constraining tunical layer. and flexi. mately 35 mmHg [12]. It has been suggested that the intracavernous therefore it is not surprising that ultrastructure fibrous framework adds strength to the tunica reflects these physiologic functions. The tunica albuginea is not present in and the end-result is an erect penis. diabetes. These sinusoids are larger centrally and partial pressure of oxygen measuring approxi- smaller toward the periphery. Partial compression of the deep dorsal septum between them is incomplete. loss of com- (postradical pelvic surgery) impairing subtunical pliance of the penile sinusoids has been observed and emissary vein compression. and perineural/periar. (4) acquired venous shunts. The glans itself has no tunical covering. intracellular events and extracellular signals. The tion [11]. . elastin. to engorge due to the presence of continued rately underneath the ischiopubic rami and then arterial inflow and venous outflow during erec- merge as they pass under the pubic arch. Smooth muscle predomi. smooth muscle relaxation occurs albuginea. ation. similar to that of the corpora except that sinu- soids are larger and the outer layer of the tunica is absent. cavernosal design reflects tone is a complex process regulated by a myriad of a functional need for rigidity. however. and myosin. activity have been reported for the corpus caver- nates. smooth muscle cells are composed of thin.1  Functional Anatomy of the Male Sex Organs 5 occlusion may result in erectile dysfunction via Alterations of the cytoskeleton for either tissue-type the following mechanisms: (1) degenerative components and/or relative quantities may be tunical changes secondary to Peyronie’s disease. The spongiosal and including the surrounding tunica albuginea. lesterolemia-induced dysregulation of collagen (3) inadequate cavernous smooth muscle relax. and is associated the fibroelastic components of the cavernous with increased deposition of collagen. during the rigid erection phase. nant types I and IV). cavernous (or corporal) which are surrounded by collagen and elastic smooth muscle is tonically contracted with a fibers. composed of actin. inter- nected sinusoids separated by smooth muscle mediate and thick filaments which are primarily trabeculae and surrounded by collagen (predomi. Within the tunica are the intercon. Modulation of the cavernous smooth muscle Similar to the tunica. bility. allowing and circumflex veins between Buck’s fascia and for neurovascular communication between sides.

The three branches of the penile may diminish trabecular smooth muscle content. The the common penile artery after giving off a branch de­creased oxygen tension of arteriogenic ED to the perineum. Smooth muscle fibers damaged by vasculo. Damage to these accessory arteries during radical ing implantation of a penile prosthesis for ED prostatectomy or cystectomy may result in vascu- of varying etiologies have been shown to have logenic erectile dysfunction (ED) after surgery a decreased number of smooth muscle cells [20. dorsal artery for engorgement of the glans penis increase collagen. where the two crura merge. vesical. The helicine arteries The paired ischiocavernosus muscles originate enter into the blood sinusoids directly without from the ischial tuberosity. femoral artery. reduce cavernous smooth for tumescence of the corpus cavernosum and the muscle content. however. These venules travel in the trabeculae spongiosus muscle originates at the central perineal between the tunica and the peripheral sinusoids to . and may occasionally become the dominant or only suggesting a variety of pathological mechanisms arterial supply to the corpus cavernosum [19]. the cavernous artery gives off many helicine arteries. Diabetes may com. obturator.2) chain globular heads and actin. is the main source of arterial calcium. and insert into the infero-medial surface the penile skin is dependent upon the right and of the corpora. but the primary mechanism is the interaction between actin and myosin. and/or femoral arteries. bulbourethral. Patients undergo. The bulbospongiosus muscle has primarily regulated by sarcoplasmic-free calcium. 21]. Distally. Shamloul Further.6 A. an important role in the ejaculation of semen. during erection. tion demonstrate similar ultrastructural changes. 1. These helicine arteries are contracted and Associated Musculature tortuous in the flaccid state and become dilated and straight during erection. iliac. The ischiocavernosus muscles function primarily The venous drainage from the three corpora to allow the corpora cavernosa to obtain very originates in small venules leading from the periph- high intracorporal pressures that would not be eral sinusoids immediately beneath the tunica possible with arterial pressure alone. covers the urethral bulb and corpus overall composition to be in-between aortic (tonic) spongiosum. which supply the trabecular erectile tissue and the sinu- soids. The internal pudendal artery becomes and sinusoidal endothelial changes [16]. and inserts into the midline.J. cover the proximal traversing a capillary bed. Bella and R. thicken the basal lamina. a branch of the Relaxation occurs with a decrease in cytosolic internal iliac artery. and cavern- leading to venous leakage. DiSanto and associates have reported tendon. Each of the filament types has a specific role. Nerve and bladder smooth muscle (phasic) [14]. The cavernous time of radical prostatectomy may also decrease artery enters the corpus cavernosum at the hilum the levels of cavernous smooth muscle while of the penis. Along its course. The internal pudendal artery. In many instances. The bulbourethral artery supplies lial cells [16. Nerve supply of these muscles is left external pudendal arteries that arise from the from the perineal branch of the pudendal nerve. compromising the the three branches join to form a vascular ring erectile process [18]. The blood supply to corpora. Cavernous nerve injury at the the bulb and corpus spongiosum. supply of this muscle is through a branch of the Smooth muscle contraction and relaxation is perineal nerve. near the glans. blood supply to the penis. with common endpoints [16]. ous arteries. The bulbo. accessory arteries arise from the external genic or neurogenic causes of erectile dysfunc. albuginea. The cavernous artery is responsible promise contractility. and cause the loss of endothe. artery are the dorsal. 17]. Contractile tone is conferred by cross-bridges linking regulatory myosin light Penile Vascular Anatomy (Fig. tone is main- tained with minimal expenditure of energy [15]. increasing collagen content.

Usually. a single vein. veins. corpus spongio- through multiple superficial veins that run sum. the inea. These veins the corpus cavernosum and spongiosum drain join the periurethral veins from the urethral dorsally to the deep dorsal. In the pendulous penis. runs dorsal vein. which in turn drains into the upward behind the symphysis pubis to join saphenous veins. The skin and subcutaneous tissue drain drainage of the glans penis. the proximal corpora cavernosa and join to 2. and ventrally to the periurethral as the emissary veins. Occasionally. Outside the tunica albug. emissary veins from form cavernous and crural veins. but some- penis to form a single (or paired) superficial times more than one deep dorsal vein. the superficial the periprostatic venous plexus. (b) venous anatomy of the penis. Beginning at the coronal sulcus. and distal two-thirds of the corpora subcutaneously and unite near the root of the cavernosa. the venous drainage is as follows: prominent deep dorsal vein is the main venous 1.1  Functional Anatomy of the Male Sex Organs 7 Fig. Emissary veins from the infrapubic penis drain corpora cavernosa. laterally to the bulb to form the internal pudendal veins.2  (a) Arterial anatomy of the penis. dorsal vein may also drain a portion of the 3. . 1. and (c) dorsal venous plexus form the subtunical venular plexus before exiting circumflex.

The nomic nerves. Lymphatics of the glans and penile urethra pass deep to Buck’s fascia and drain into both superficial and deep inguinal nodes. The somatic dorsal nerves primar- urethra is essentially a potential canal that opens ily provide sensory innervation for the penile skin only during micturition and has a characteristic and glans.J. Bella and R. The pudendal nerve gives 1.8 A. Urethra (Fig. Shamloul Lymphatics Sympathetic autonomic fibers derive from the hypogastric plexus and join parasympathetic autonomic fibers from S2–4 in the pelvic plexus.3) Innervation The male urethra is a canal that extends from the bladder neck to the external urethral meatus passing through the substance of the corpus The penis is supplied by both somatic and auto- spongiosum. bulbocavernosus muscles whose contraction help The prostatic urethra is approximately 3 cm in to increase the rigidity of erection. The pudendal length and considered to be the widest and nerve also gives a sensory branch that supplies most distensible part of the canal. perineum. dal vessels. 1. and thus contain both sympa- via channels alongside superficial external puden- thetic and parasympathetic fibers. eventually becoming divided into the following parts: the pudendal nerve and entering the spinal cord via S2–4 nerve roots. and approximately follow the course S-shaped course. Lymphatics of the prepuce and penile shaft Cavernous nerves represent the penile branches converge dorsally.3  Cross-sectional anatomy of the pelvis . 1. It is about 20–22 cm in length. Posterior urethra: This is composed of the pro- off a motor branch to the ischiocavernosus and static urethra and the membranous urethra. The male urethra is further of the dorsal penile arteries. and the rectum. from the neck of the bladder passing through Fig. and then drain into both right- of the pelvic plexus that ramify once piercing the and left-sided superficial inguinal lymph nodes corporal bodies. It extends the penis.

vasculosa.5 cm) skeletal muscle part of the mem­branous ure. genital diaphragm and it is a muscular organ Each testis is about 4. namely the the inguinal canal within the spermatic cord . is considered pathological and may predispose to laris” to terminate at the external meatus. about 3 cm wide (average of 2–3. By the time of birth both testes should lous urethra. 3. the part of the urethra as it passes through the uro. The bulbous urethra is the be completely descended in the scrotum. while the penile testis suspended high in the scrotum (at the scro- urethra is the distal-free part of the anterior tal neck) or having an inguinal canal location. The outer layer is the tunica to the external urethral meatus at the tip of the vaginalis. The membranous urethra is the thickest glands and hair but no subcutaneous fat). The vol- thra forms the external (voluntary) sphincter. and the inner layer is the tunica the bulbous urethra and the penile or pendu. It consists The mediastinum testis acts as a supporting struc- of involuntary nonstriated muscles and is ture to the testicular vessels and ducts that pass supplied by autonomic nerve supply. A transverse lie of the testis a small dilatation named the “fossa navicu. the ureter (supplying it) and then passes through matic cord has three fascial layers. The penile urethra ends by absent). Its posterior wall shows an elevation spermatic cord contains vascular and nonvascu- termed the “veromontanum” which is related lar structures. The sper.5  cm long (average of with both smooth and skeletal muscles.5 cm). tains a number of seminiferous tubules that harbor the germ cells. The thra. dartos muscle and the dartos fascia. within the mem- within the aforementioned framework. the intermediate layer is the thickened glans penis. in adolescent boys [23]. It is light branous urethra is formed of voluntary brown in color and is divided into several hun- striated muscles and supplied by somatic dred lobules by fibrous septa. Anterior urethra:  This portion is about 15-cm Generally. or urethra and is the continuation of the proxi. external spermatic fascia. It is a branch from the abdominal aorta originating just below the root The male testes are ovoid organs suspended by of the renal artery. The parenchyma of the testis exists (b) The external sphincter. the recurrent attacks of testicular torsion especially narrowest point of the entire canal. proximal part of the anterior urethra and is Abnormal testicular positions are not uncommon surrounded by the bulb of the penis and the and can affect one or both testes. the most important of which is the to three important structures: the prostatic utri. and 3 cm in its anteroposterior diameter. the cremasteric muscle static neck by becoming the membranous ure. Each lobule con- nerve supply [11]. long extending from the membranous urethra called the tunics. This may include bulbospongiosus muscle. The testicular artery is main arterial blood Testis supply to the testis. way) or less commonly impalpable (abnormal or physis pubis. Urethral sphincters The inner aspect of the tunica albuginea gives off a number of thin septa that converge on the (a) The internal sphincter controls the bladder posterior aspect of the testis itself to form a mass neck and the prostatic urethra above the of fibrous tissue known as the mediastinum testis. being ectopic (not in the normal descent path- mal bulbar urethra at the lowest level of sym. The anterior urethra is formed by tunica albuginea. paired ejaculatory ducts. opening of the ejaculatory ducts. The testicular orientation is usually ver- passing through the glans penis where it forms tical in the scrotum. and fascia.5–5. and the prostatic of an outer thin skin layer (containing sebaceous ducts.1  Functional Anatomy of the Male Sex Organs 9 the substance of the prostate to end at the pro. vas deferens. ume of each testis ranges from 15 to 25 mL [22]. the supporting Sertoli cells and are further surrounded by the interstitium [24]. and the internal spermatic fascia. The testicular artery crosses the spermatic cord within the scrotum. 2. The scrotum itself is a sac formed cle. through it. the testis has three main coverings. The 3.

drain the marginalis of the epididymis. Finally. Further blood follows: the seminiferous tubules in the testis supply to the testis comes from the vasal artery form a network in the mediastinum testis named which originates from the inferior vesical artery. Finally. albuginea of the testes with autonomic pain receptors It begins as a continuation of the lower end of the while the testicular parenchyma itself is devoid of epididymal duct at the level of the epididymal any pain receptors. the rete testis. the body (intermediate). and the tail (lower of vessels that supplies the testis through the part). The epididymal aspect starts at the epididymal tail The human epididymis is a comma-shaped struc. supplying the tunica about 45  cm long and 2. tail and ends by uniting with the duct of the seminal vesicle to form the ejaculatory duct that opens on the veromontanum on the prostatic urethra [25]. The vas deferens runs a long course Epididymis that can be divided into five main segments. Bella and R. From this rete testis arise (12–20) supplying mainly the vas deferens. The anterior group. the mediastinum testis of the testis by a fibrous remnant of the guber- is considered to be the most vascular part of the naculums known as the epididymal ligament. The testicular artery also gives a branch to Microscopically. teric (external spermatic artery) and vasal arter- The middle group of the testicular venous ies are present. spermatic vein) that drains into the left renal vein tric vein [25]. the posterior veins. Nerve supply to the testes primarily originates high in the spinal cord Vas Deferens from the 10th and 11th thoracic segments. made up of the vasal veins. additional collaterals from the cremas- drains into the inferior vena cava [25]. and runs a winding course within the tunica vag- ture that overlies the superior and posterior sur.5  mm in diameter. It is formed of the head (upper Following that. Shamloul where it ends by forming a convoluted network part). this epididymal duct ends in passes high through this plexus. epididymis that is 6  m long enclosed within a ticular artery.J.10 A. This pampiniform plexus constitute connective tissue sheath in the body of the the main venous drainage of the testis. These nerves accompany the testicular artery through its The human vas deferens is a muscular tube of passage in the inguinal canal. The arterial supply of the epididymis nal inguinal ring where they become the single comes from a branch from the testicular artery testicular vein. becomes around the testicular artery. made up of the cremasteric veins. they testicular veins. efferent ductules (vasa efferentia) that pass from Testicular venous drainage can be divided into the testis to the epididymis to form the epididy- three main groups. The tail is attached firmly to the lower pole mediastinum testis. while the right testicular vein the aorta. the epididymis is formed as the upper part of the epididymis. its branches the tail of the epididymis by joining the vas def- decrease gradually until passing through the exter. (on the left side) and the inferior vena cava (on The intratesticular lymph ducts originate in the the right side). and may join the vas and the epididymis into the prostatic and the cremasteric veins and the pampiniform plexus of vesical venous plexuses. As blood epididymis. The left testicular vein drains into (internal spermatic artery) that is a branch from the left renal vein. testicular interstitium and ascend inside the sper- matic cord to drain finally into the paraortic lymph nodes at the lumbar region. inalis along the posterior aspect of the testis. Thus. the scrotal portion runs a straight . faces of the testis. These veins fuse in separated from the spermatic cord at the external the inguinal canal to form the testicular (internal inguinal ring and drains into the inferior epigas. forming a network of about 15 veins group. testis. Venous drainage is from the vena drainage. erens. Then. is formed by the pampiniform unite to form the convoluted duct of the plexus which is closely associated with the tes. called the mal lobules in the epididymal head.

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and labia extends from the perineum superiorly and poste- minora (Fig. USA aspect of the uterus.1007/978-1-60761-916-1_2. the vagina at approximately a 90° angle.C.2). elongated. The majority mately 1  cm superior to the urethral meatus. Yang Keywords  Anatomy • Vagina • Clitoris • Uterus covered by pubic hair. The posterior aspects of the labia minora fuse in the midline at the lower aspect of the introitus. approxi- role rather than sexual responsiveness. Seattle. known as pathophysiology of sexual function. The urethra is located immediately superior to the introitus. there is a ing folds of tissue forming the lateral boundar- growing awareness that while sharing some of the ies of the vulva. Only the has long been on understanding its reproductive glans clitoris is visible externally. Loops of intestine are found superior C. The mons pubis is an area of riorly toward the cervix. with the bulk of their tissue The emphasis of the study of the female sex organs lateral to the vaginal walls (Fig.Chapter 2 Functional Anatomy of the Female Sex Organs Van Anh T. Harborview Medical Center. The uterus typically is positioned posterior and supe- rior to the bladder. ine tubes extend laterally from the superior WA 98104-9868. J. tubes. uterine The external genitalia are referred to collec. The medial aspects of the labia same anatomical structures and hormonal milieu. the uterus (including cervix). entry to the vagina. 2. hair bear- from the context of reproduction. 2. which run bilaterally under the inferior pubic rami. 2. with unique physiological responses. Posterior to the vagina is the rectum. The body of the clitoris extends into the mons for several centimeters. Current Clinical Urology. (eds. which are sexual function and fertility/reproductive function thin folds of skin outlining the introitus.P. University of Washington. Cancer and Sexual Health.1). which protrudes into fatty tissue overlying the pubic symphysis. clitoris and bulbs.3). or are distinct.). The anterior aspects of the The following is a brief presentation of the labia minora split and fuse with the ventral anatomy and histology of the female sex organs. labia majora. 13 DOI 10. before bifurcating into the crura. aspect (or frenulum) of the glans clitoris and from the perspective of understanding the also unite over the glans as a hood. Mulhall et al. The vagina is imme- tively as the vulva and consists of the mons diately posterior to the urethra and bladder and pubis. Introduction Between the crura lie the clitoral bulbs. Ginger and Claire C. Yet. the clitoral prepuce. © Springer Science+Business Media. draped over the urethra. General Structural Relationships The internal genitalia are comprised of the vagina. and ovaries (Fig. of anatomic descriptions for these organs have been The labia majora are fatty. LLC 2011 . The ovaries and uter- Department of Urology. majora fuse with the labia minora. Yang (*) and posterior to the uterus.

2  Axial view of female genitalia. 2. labia minora.  2. and urethra reveals them to contain specialized vascular tissues that are sexually responsive [1] and consist of two histologically distinct types of vascular tissue.4). MD) in length.1  Female external genitalia (premenopausal vessels are dispersed within a fibrous matrix. 2. the corpora cavernosa.4). 2. Maravilla. the erec- tile tissues are trabecular. The clitoris is comprised of two erectile bodies. Crus The clitoral body and the crura can be 10 cm or clitoral crus. there nance image.C. The erectile tissue of the clitoris and bulbs is very similar to that of the male corpora cavern- osa and corpus spongiosum. woman) (Image from with only a minimal amount of smooth muscle. of the clitoris is hidden by the mons pubis.T. structures. The body is the convergence of two corpora. Under GNU Free Docu­ mentation License. wiki/File:Womans_vulva. the labia minora and glans clitoris are composed of nonerectile vascular tissue in which the blood Fig. Each of the corpora cavernosa is surrounded by a thick fibro-elastic tunica albuginea (Fig.  2. IT ischial tuberosity more in length with the body measuring 5–7 cm (image courtesy of Kenneth R.A. clitoral bulbs. Because the majority Fig. magnetic reso. dilated vascular spaces that are filled with blood and are spongy in appearance (Fig. On histological examination.5). (The high signal intensity of the mons and sur- rounding tissue is artifact.wikimedia.) Nonerectile.14 V.jpg. R rectum. U urethra.) Body body of clitoris. Clitoris The structure of the clitoris has been “redis­ covered” many times over the years by anatomists due to the frequent omission or misrepresenta- tion of the organ in historical and contemporary anatomical texts. Gross examination of these structures demon- strate large. In contrast to the clitoral and bulbar erectile tissue. with smooth muscle underneath the epithelium of the vascular spaces. Yang External Genital Anatomy Gross anatomical and histological study of the clitoris. and the crura are the extensions of the corpora beneath the descending pubic rami. The first type is the trabeculated erectile tissue seen in the clitoris and the bulbs. . Ginger and C. sexually responsive vascular tissue is also found surrounding the urethral lumen and within the walls of the vagina (see below). The high intensity signal of the clitoris and is a lack of appreciation for the substantial nature the bulbs is a function of the high blood flow within these of these erectile bodies in the vulva (Fig.

sagittal view (based on drawing by Robert Holmberg. a collec. dilated and subcutaneous tissue is tan. Right clitoral bulb stained red. (a) Gross sagittal view of indicates the approximate level of the cross-section seen external genitalia. (b) Axial view ing anteriorly into mons pubis and prepuce (glans not vis.2  Functional Anatomy of the Female Sex Organs 15 Fig. The large. Vertical line lumen. Pars intermedia.3  Female internal genitalia. is bulbar tissue draped over the urethral lumen.  2. Clitoris is inked blue.5 cm .4  Clitoris and bulb. Skin appears dark brown. with body extend. 2. WA) Fig.4b. in adjacent image 1. tile tissue with residual pooled blood. Metal probe the anterior vaginal wall is seen beneath the urethral placed through urethral lumen (not visible). Seattle. Width of clitoral body approximately 1. vascular spaces are apparent in the clitoral body and the tion of vessels between the clitoral body and urethra. Centimeter ruler. The rugae of stained green. The darker colored tissue is erec- ible). and right crus amputated. of genital cross-section.

The clitoris appears to be a purely sen- sory organ [2]. Bar = 1 mm The glans clitoris rests as a fibrovascular cap at the tip of the clitoral body.6). On histological examination. 2. thus differentiat- ing it from the erectile tissue of the clitoris and bulbs. arrow nerve fascicles.T. particularly on its dorsal surface. veins.16 V. 2.A. Just beneath the epithelium of the glans is an abun- dance of neural elements. form the clitoral body. Collagen/connective tissue corpora.  2. The two corpora cavernosa converge to tion of arteries. including nerve fibers and receptors. smooth muscle (and residual pooled the tunica. tissue. the glans clitoris is richly innervated and is an important mediator of sensory input for sexual arousal (Fig. Surrounding stained dark blue. The bulbs lie flanking the urethra . Neural elements are stained brown. Despite its diminutive size. of the erectile tissue allows for engorgement and The bulbous head of the glans is surrounded by preputial expansion during sexual arousal. nerves.C. They are surrounded by a fibrous Arrowhead artery. Dilated vascular spaces comprise the erectile tissue of the Masson’s trichrome stain.4). tunica albuginea and separated by a fibrous septum. the clitoral tis- sue is composed of large vascular spaces with mainly vascular epithelium and smooth muscle Fig. is a collec- blood) stained red. Yang Fig. Ginger and C.6  Longitudinal section of clitoral glans and body. Unlike its male counterpart. but The clitoral bulbs drape over the urethra (similar are more closely related to the clitoris than the to a saddle bag) with the two globular bulbs lying vestibule [3]. interspersed throughout.5  Midshaft cross-section of clitoral body. Bar = 1 mm Bulbs inferior to the clitoral body (Fig. the glans clitoris lacks smooth mus- cle within its fibrovascular cap. and supporting tissue. 2. The bulbs are also referred to as the vestibular bulbs. some filled with residual corpuscles. The trabecular nature S100 antibody stain. asterisk vein.

while the bulbs have more subcutaneous tissue of the labia majora consists prominent fibro-elastic tissue and smooth mus.8). blood flow during sexual arousal. Numerous vascular structures of varying sizes are surrounded by collagenous connective tissue.2  Functional Anatomy of the Female Sex Organs 17 and vagina and sit recessed within the vestibule.7  Clitoral bulb. The expansion Labia Minora The labia minora are folds of tissue between the introitus and labia majora (Fig. 2. the bulbs become vessels. hairless. and unlike the labia majora. and the vaginal introitus. mostly of fat. glans clitoris. . smooth volumes of blood during arousal.7). dantly present. The tissue immedi- ately deep to the epithelium is nontrabecular (nonerectile) vascular tissue. is comprised engorgement and enlargement during sexual of trabecular vascular spaces designed to accommodate arousal. of the bulbs and their subsequent encroachment They do not surround the introitus as suggested on the introital opening may contribute to a sen- by some texts. but the bulbs do not com. Elastin is abun- muscle (and residual pooled blood) stained red. sparse nerves. They enclose the labia clitoris.1). and blood and lymphatic During sexual arousal. Vascular structures in the labia minora seen to the right side of the image. In contrast to the clitoris. 2. not smooth muscle (Fig. Labia Majora The bulbs are considered the equivalent of the male spongiosum. Trauma due to child- birth and other types of irritation of the labia minora can result in asymmetric hypertrophy. The erec. The histologic that extend between the mons pubis and the features of the bulb are similar to that of the perineal body (Fig. rather than active increase in blood cant enlargement of the organ with increased flow as occurs in the other parts of the vulva. The labia majora change with sexual engorged with blood. The size of the bulb varies between individuals and may be dependent on age and estrogenization.1). Collagen/connective tissue stained dark blue. arousal. Masson’s trichrome stain. bundles. There is no tunica albuginea sation of genital engorgement. pigmented skin folds. This skin is generally smooth. There can be some degree of atrophy with decreased estrogenization. The fibro-elastic tissue. They also contain the terminations cle bundles lining the vascular spaces of the round ligaments. slightly less smooth muscle and interstitial They are hair bearing. This is in distinc- tion to the trabecular vascular tissue of the clito- ris and bulbs. there is no surrounding tunica albuginea. presumably to allow for labial tile tissue of the bulb. congestion. 2.  2. since there is very little smooth muscle large volumes of blood during sexual arousal. The labia majora are two elongated folds of skin pletely encircle the urethra. some smooth muscle (Fig. from what appears to be passive vaso- sue and the absence of a tunica allow for signifi. The erectile tissue of the clitoris has minora. Bar = 1 mm are more numerous than in the labia majora. The bulbar trabecular tis. and no trabecular erectile tissue within the labia Skeletal muscle of the bulbospongiosus muscle (BSM) is minora. enveloping the erectile tissue. like that of the clitoris. designed to accommodate large Fig. they contain very little adipose. 2. There is great variation in the size and shape of the labia minora between individuals. and pig- mented.

interspersed with elastin fibers meatus. central core of neural elements which is present which becomes transitional epithelium as it along the length of each labium.18 V. such as vulvec- tomy. and certain forms of female circumcision. elastic Masson’s trichrome stain. V vagina. R rectum. nonerectile vascular tissue. Exenterative procedures. S100 antibody stain. there is good reason to believe that alteration of the labia minora can change sexual responsive- ness. Vessels are apparent in by asterisks).8  Labium minus. The rich innervation of the labium minus is evident with the staining of neural elements.C.9).10  Urethra. central nervous system. axial The substance of the labium minus is filled primarily with cross-section approximately 3  cm proximal to urethral collagen (dark blue stain). This is in contrast to the labia majora. Dilated vascular spaces are evident.  2. The collapsed vagina is seen many filled with red corpuscles (two examples designated between the urethra and rectum. one identified by arrowheads. There is a that is lined by stratified squamous epithelium.  2. It is a rugated muscular tube apparent within the labia (Fig. can have a deleterious effect on the sexual response by ablating the sub- strate through which sexual sensations enter the Fig.T. Ginger and C.10) and engorges with sexual . Fig.A. as well as evi- dence that the tissue is sexually responsive [4]. also considered specimen. reduction labiaplasty. The dark tissue surrounding the urethral lumen is (black wavy lines). U urethral lumen. 2. vagina. rectum gross specimen. This neural core approaches the bladder. Bar = 1 cm engorgement occurs in response to sexual arousal. The distal urethra is appears to travel alongside the major vascular flanked by the erectile tissue of the clitoral bulbs. 2. structures within the labium minus and is the The urethral tissue bears a nonerectile vascular neurovascular substrate through which labial pattern (Fig. The labium major specimen is fractured due to processing. Given the generous vascular and innervation patterns within the labia minora. Large nerve trunks traverse through this the substance of the vaginal walls. Urethra Bar = 1 mm The urethra is a midline structure and sits deep Neural fibers and receptors are abundantly within the introitus. 2. where nerve fibers and receptors are sparse. Yang Fig. Bar = 1 mm nonerectile vascular tissue.9  Labium minus and labium major cross-section.

and perineal Genitalia skin. innervation to the perirectal skin. the inferior rectal nerve. which then drains into the vesi- cal venous plexus within the pelvis. or hypogastric. Asterisk desig- nates urethral lumen. posterior labial in our lab have shown the DNC to run in parallel . Bar = 0. ter. Some of these glands stain posi- tively for prostate specific antigen (PSA) [5]. The pudendal nerve. an area that in talia are the dorsal nerve of the clitoris (DNC) some women is particularly sensitive to tactile and perineal nerve. body. of the DNC. artery to the bulb. divides into a series of anterior labial branches to supply the labia majora and Fig. There are paraurethral glands along the length of the lumen. the anal sphinc- ings to distinguish it from other parts of the ure.1 mm drainage of the labial skin is via the external pudendal vein. The venous coalesced into any macroscopic organ. the perineal artery. Innervation of the External Genitalia leading some to state that this area is homologous to the male prostate.12). the internal iliac. pelvic floor. innervating the clitoris (crura. A third branch of the puden- stimulation. 2. Anatomic dissections of the clitoris. introitus. with less vascular structures the clitoral bulb. The DNC is exclusively a sensory nerve. are not from the internal pudendal artery. A branch of the femoral artery. exocrine function of PSA is to liquefy semen).11) and do not have any recognizable The innervation of the external genitalia involves endocrine or exocrine function in women (the both somatic and autonomic fibers (Fig. The urethral tis- labia minora. There is variation in tissue vas- arousal. provides area have not identified gross or histological find. artery. A secondary source of blood supply to the external genitalia arises from the femoral artery. However. The external pudendal artery sue surrounding the lumen includes occasional glands enters laterally from the thigh and tracks towards that stain positively (brown) for prostate-specific antigen the vulva to join with the posterior labial arteries (PSA). and there is still some controversy ple variable branches. as well as motor innervation to the external urethral sphincter. is the main source of somatic lying the midurethra has been identified as the innervation and its terminal branches to the geni- Grafenberg spot (or “G-spot”). Small branches also supply the vaginal wall [7]. which drains into the greater saphenous vein. The glandular elements. It is surrounded by the erectile tissue of cularity with age. the glands are iso- lated (Fig. the labia Blood Supply of the External minora. and glans). the external pudendal artery. including the dorsal artery regarding its exact course. however.2  Functional Anatomy of the Female Sex Organs 19 artery. nal segments S2–4. and much of the pelvic floor The main source of blood supply for the pelvis is skeletal musculature. but the urethra itself contains no found in older women compared to younger erectile tissue. women. From Multiple studies have examined the pathway this. which is centrally located in the erectile tissue of the corpora cavernosa. as well as the deep artery of the clitoris.11  Periurethral gland. Numerous anatomical studies of the dal nerve. arising primarily from spi- The region of the anterior wall of the vagina over. PSA stain. distal urethra. the internal pudendal artery gives off multi. The venous drainage of the clitoris and bulb is via the deep dorsal vein.  2. The perineal nerve provides sensory innervation to parts of the labia majora. 2. and parts of the musculature of the posterior thra or vaginal wall [6].

composed of smooth muscle fibers description of the spinal origins of the autonomic disposed both longitudinally and circularly. (A more detailed cular layer. just lateral to the midline.  2. The vaginal wall consists from the caudad thoracic spinal segments and of three layers: (1) the stratified squamous the sacral spinal segments innervate the vessels nonkeratinized epithelium and an underlying and smooth muscle of the erectile and nonerec. The suspensory ligament is an acellular ligament that pathetic innervation is derived from T10 to T12.20 V. and fibers is described in section “Innervation of the (3) the adventitia. Parts of the labia majora are innervated by the anterior labial branches of the The vagina is a flattened fibromuscular tube ilioinguinal nerve. White strands of the ligament are seen. (2) the mus- tile vascular tissue of the vulva.T. 2. secondary elevations called sympathetic and parasympathetic fibers arising rugae extend laterally. Bar = 5 mm to the crura under the inferior pubic symphysis prior to ascending at the pubic ramus and pro.13). and the attaches the body of the clitoris to the symphysis pubis. Within the strands of the suspensory liga- drawing by Robert Holmberg.10). primarily through the pudendal nerve (S2–4). While the DNC is visible to the naked A longitudinal ridge is present along the mucosal eye. . gross view. small to identify without magnification. lamina propria of connective tissue.”) blends with the surrounding fascia. the fibers of the cavernous nerves are too surface of both the anterior and posterior walls.13  Suspensory ligament and clitoris. Internal Genital Anatomy ceeding within the suspensory ligament towards the glans clitoris (unpublished data) (Fig. WA) ment. surrounded by Not shown are autonomic fibers from the pelvic plexus to adipose.A. 2. whose anterior and posterior walls are collapsed The cavernous nerves carry the autonomic onto each other. Other areas of the vulva are innervated via Vagina nonpudendal fibers. extending from the introitus to innervation to the erectile tissue of the clitoris the fornices that surround the cervix (Fig. The ligament attaches to the dorsal aspect of the the erectile tissue of the clitoris and bulbs (based on clitoral body. Ginger and C.12  General pattern of genital innervation. These from these ridges. Seattle. Yang Fig. The sym. 2. CC corpus cavernosum. The fascicles occur bilaterally. parasympathetic innervation is derived from S2 to S4. The somatic innervation of the female sex organs is mediated Fig. nerve fascicles of the DNC travel toward the glans (cut ends of the nerves designated by arrowheads). a dense connective tissue that Internal Genitalia.C. and bulbs.

when if there is no developing embryo implanted estrogen levels are relatively low. the pelvis by an arrangement of ligaments and rectovaginal. There is no discrete vaginal “sphincter. uterus within the pelvis.” poorly defined owing to overlap between adja- although the pelvic floor muscles in aggregate cent layers. the basic anatomy and his- course. pear-shaped organ. control of the ovarian hormones. shape. nance of normal size and function in myometrial smooth muscle cells. but their boundaries are muscles. membrane. and (3) the serosa. Above this area are several layers of polyhedral cells that appear to be connected Uterine Corpus (or Body) together much like those of the stratum spino- sum of the epidermis.0 or higher flow) and is regenerated again in the next after the menopause). and caused by transudation across the vaginal wall. pubococ. There is also much less menstrual cycle. more layers of cells that are flatter in appearance somewhat flattened anteroposteriorly. tology. striated skeletal musculature of the pelvic floor. sacrogenital) that also support the supported inferiorly by the pelvic floor (Fig. location. and structure as a result of in fluid production in the vagina is believed to be hormonal fluctuations. The reproductive physiol- The transudate provides the lubrication needed ogy associated with this organ is beyond the for nonpainful and nontraumatic vaginal inter. . the epithelium is during a menstrual cycle.3). it is a luxuriant mucosa Estrogen stimulates the production of glycogen with a large population of glycogen-secreting and maintains the thickness of the entire epithe. The resulting acid. most of the endome- thin and the pH is higher than in the reproductive trium is sloughed off (causing the menstrual years (neutral before puberty and 6. and the superficial and deep transverse perineal have been distinguished. of the body of the uterus is composed of three The most superficial cells are desquamated into layers: (1) the endometrium. in the context of sexual function. The serosa is the peritoneal covering of the uterus. the marked increase size. smooth muscle fibers separated by strands of cygeus. glands and a rich vascular network. This cyclic shedding and transudate formed with sexual arousal following regeneration of the endometrium is under the menopause. other circumstances. Estrogen is essential for the mainte- functionally contract the introital opening. a glandular mucous the vaginal lumen where their intracellular gly. cardinal. However. uterosacral) The uterus is a muscular structure suspended in as well as peritoneal reflections (vesicouterine. puborectalis). The myometrium consists of bundles of including the levator ani (ilioccoccygeus. As such. modate the developing ovum. scope of this chapter. Before puberty and after menopause. attached to the uterus at the fundus and Uterus body. will be The stratified squamous epithelium of the described here. connective tissue. 2. The function of the endometrium is to ity is believed to be important in protecting the provide a suitable environment for the implan- female reproductive system from infection by tation and subsequent growth of the devel- most pathogenic bacteria. lium. Above these are several The uterine corpus is a thick. adult vagina is several layers thick. There are no glands in the vaginal wall.2  Functional Anatomy of the Female Sex Organs 21 The lamina propria and connective tissue Its anatomy and histology is designed to accom- layers contain a rich supply of vascular channels. the bulbospongiosus mus. and it varies in During sexual stimulation. Four layers of smooth muscle cles. estrogen and The vaginal introitus is surrounded by the progesterone. oping embryo. age. probably by cle layer. (2) the myometrium or smooth mus- cogen is converted into lactic acid. normal vaginal bacteria flora. Four paired sets of ligaments are attached to the uterus (broad. The basal layer is a single layer of cylindrical cells with oval nuclei. round. pregnancy. The wall and accumulate glycogen in their cytoplasm.

22 V. ganglia. Within the broad ligament. Here the plexus of veins uterus and cervix do contribute to the sexual forms a series of tributaries entering the internal response. promontory. the fibers join the superior hypogas- The uterine tubes are also not considered to be tric plexus and enter the sympathetic chain via sexually responsive. ing laterally in the base of the broad ligament Although it is considered primarily a repro. and vesical arteries. In the uterine isthmus (the transition of artery. A longi. Sensory fibers from Ovaries and Uterine Tubes the uterine body descend in the parametrium (the lateral extension of the uterine subserosal connec- The ovaries are the germinal and endocrine tive tissue into the broad ligament) to join other glands of the female. following the uterine artery before reaching the ductive organ. according to studies that demonstrate improved sexual functioning following hysterectomy for benign disease.A. Below this the ilium. It forms with the bifurcation of the com- the corpus to the cervix). nonkera. From the sympathetic cussed in this chapter. 11 The exact mechanisms are Innervation of the Internal Genitalia unknown to explain sexual function changes fol- lowing uterine surgery. the peritoneal reflection. occurs. there is clinical evidence that the lateral pelvic wall. uterine. before entering the response and are typically not thought to inferior hypogastric plexus. the uterine artery gives branches to the arranged in a series of folds and ridges. from each of of the uterus until the uterine artery anastomoses these. the uterine lumen nar. The external gives off a series of visceral branches including os at the lower end of the cervix provides com. The uterine vein is usually plexiform. mon iliac artery at the junction of the sacrum and rows down to form the internal os. cours- tinizing epithelium. The uterus and vagina are innervated by auto- nomic and visceral afferent (sensory) fibers. the internal iliac (hypogastric) muscle. the internal iliac artery vical canal (or endocervical canal). vagina and cervix.12) the alteration of local nerve [8] and blood supply. Ginger and C. the lumen widens slightly to form the cer. Ascending the sacral undergo structural changes with sexual arousal. contributing to the hor. Before reaching Inside the cervix. 2. The ectocervix is with the ovarian artery at the uterotubal the part of the cervix that projects into the vagina junction. small folds run laterally. at the vagina. and is covered by stratified squamous.T. tudinal ridge runs down the anterior wall and a series of arterial branches is given to the body another down the posterior wall. which run along the uterine arteries. white rami communicans conduct fibers . They will not be dis.C. or by changing anatomical relationships. Yang Cervix Blood Supply of the Internal Genitalia The cervix is located at the inferior aspect of the uterus and is generally 2–3 cm in length.10. It con- sists primarily of dense collagenous connective The pelvic organs are all supplied by a single tissue. lumbar splanchnic nerves. the base of the broad ligament. the endocervical mucosa is the uterus. their relative contributions iliac vein. 9 However. the rectal. vena cava. which in turn empties into the inferior to sexual satisfaction may not be significant.8. whether it is caused by (see Fig. fibers from the cervix to form a large plexus in the monal milieu in which the sexual response paracervical region called the uterovaginal plexus. Descending in the lateral pelvis below point. Only about 15% of its substance is smooth arterial trunk. It is not known if the ovaries have any These fibers then comingle with visceral afferents other function with regard to the sexual from other pelvic viscera. These munication between the lumen of the cervix and course medially to enter the endopelvic space.

108(5):423–5. or A comparative immunohistochemical study of indirectly by disruption of the vascular. but may introitus is supplied by sensory fibers of the contribute to the sensory input required to gen- pudendal nerve. et al. et  al. as well as sympathetic motor fibers that structures are not known to have direct motor enter from the sympathetic chain. two thirds of the vagina is not somatically inner. Homology between the this translates to improved postoperative sexual female paraurethral (Skene’s) glands and the prostate. editors.159(6):1892–7. Lowry TS. Louis. In: Lowry TP. Yang CC.185(2):359–62. Anatomical basis for lar tissue of the genitalia. MD provided ments. Biol. Campbell B. not involved in the surgical dissection. Kenter GG. Anatomical relation- showed that the anterior part of the plexus was ship between urethra and clitoris. Suh DD. J Psychosom small nerves on the medial border of the inferior Obstet Gynecol. disrupting the major part of the hypogas. 4. hypogastric plexus in both techniques. The anatomy of the distal vagina: towards unity. particularly in regard affect genital sensation? Eur J Obstet Gynecol Reprod to their role in the sexual response.25:153–62. tissue of the vulva. Yang CC. O’Connell HE. particularly of the nerve-sparing radical hysterectomy: immunohis- vulva. neural. Lab Med. The clitoris.5(8):1883–91. rior border of the surgical margin. terectomy has not been definitively determined. The G-spot: a modern gynecologic myth. the nerves after the nerve-sparing procedure 3.119(2):242–5. following the nerve-sparing technique of hysterectomy. Yarnitsky D. Contrary to many texts. et al. Acknowledgement  Christopher Cold. vated. Arch Pathol functioning in women with a nerve-sparing hys. MRI of female genital and of the vesicouterine ligament disrupted only pelvic organs during sexual arousal. assistance with gross and histologic sections. Dissection 1998.2  Functional Anatomy of the Female Sex Organs 23 to the dorsal roots of spinal nerves T10–12. p. Cold CJ. or the pelvic autonomic nerves to the uterus revealed hormonal supply to the genitalia. 2001. 2004. the pertinent genital anatomy. tric nerve. 2005. The engorgement can occur during arousal. Whether 5. tion is dependent on a clear understanding of 7. Am J Obstet Gynecol. Division of the cardinal ligaments in the standard procedure identified the inferior 1. et  al. The anterior 2. 1976. in female genital anatomy has clarified the 8. Eizenberg N. References rupted [9]. O’Connell HE. Malignancies involving the genital structures. Lowenstein L. Maas CP. The vaginal responses during the sexual response. Jagirdar J. 1984. Other genital directly. Immunohistochemical demonstration. Understanding the causes of sexual dysfunc. Tepper SL. Hutson JM. Recent research 2008. Sexually responsive vascular hypogastric plexus running into the most poste. et al. Does hysterectomy nature of these structures. and both motor fibers from sacral roots that enter the pelvis types are sexually responsive. Warren part of the plexus was disrupted. Neurophysiology of the clitoris. However. et al. BJU Int. These uterovaginal plexus also includes parasympathetic tissues are erectile and nonerectile. The vascu. can affect the distal vagina appear to have somatic sensation. 2006. J Urol. et al. sexual response by direct injury or ablation. only the medial branches of the hypogastric nerve appeared dis. 9. the lower erate and propagate the sexual reflexes.97(4):766–72. only the introitus and the first 1–2 cm of the or the treatment of malignancies. that standard technique of radical hysterectomy results in transsection of the uterosacral liga. is the anatomic substrate by which pelvic . 35–74. Hines TM. J Sex Med. Dissection of Green: St. 6.

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It and erectile tissues and sympathetic blood flow drives our sexual fantasies. produce increases in libido. (eds. compels us to seek out from the heart to striated and smooth muscles and evaluate sexual incentives. desire. Delineating the neural mechanisms that underlie Introduction these aspects of sexual function has been the focus of recent research in animals and humans. or engage in other forms of Sexual arousal also includes a central component sex play. docrine mechanisms. etc. 3. these aspects stances that stimulate the autonomic nervous of sexual function feed back on mechanisms of system [2]. be defined as increased autonomic activation scious reflection of sexual motivation. However. Fig. copulate. masturbate. heart rate. The Latin root refers specifically to Sexual Arousal sexual lust. a term that conjures images of highly motivated behavior.Chapter 3 Physiology of Libido James G.G. regulates our levels that participate in sexual responses (e.1007/978-1-60761-916-1_3. Canada which is often characterized by “high” libido in J. Pfaus Keywords  Libido • Arousal • Nitric oxide arousal. Concordia University. Libido is observed in the strength of desire and responding toward a sexual Physiological sexual arousal in all animals can incentive. Fig.). Cancer and Sexual Health. 3. it is also modulated by experiences following the use of psychomotor stimulant and expectations. 25 DOI 10. © Springer Science+Business Media.1a) or decrease • Medial preoptic area • Paraventricular nucleus (as in the case of reward or inhibition. High sympathetic activation is an impor- Department of Psychology. which we that prepares the body for sexual activity. respond to sexual incentives.. Center for Studies in Behavioral Neurobiology. and therefore can be regarded as a con. tant antecedent of premature ejaculation [3]. This can occur mone actions. such as alterations in brain Increases in general sympathetic outflow neurochemical function set forth by steroid hor. 7141 Sherbrooke West. these putative increases in motivation.). either to increase (as in the case of libido are most likely to occur in sexually-spe- cific situations. Montréal. Although sexual motivation is often that increases the psychological preparedness to viewed as an internal process built upon neuroen. In turn. pupil dilation.1b) the expression of sexual interest or libido.P. Libido has always been associated with sexual motivation.g. that contain psychoactive alkaloids or other sub- desire. learned patterns of behavior and drugs [1]. Mulhall et al. and inhibition. reward. QC H4B 1R6. Pfaus (*) ment. or ingestion of herbal “aphrodisiacs” underlying neural activity related to sexual arousal. indicating an interaction between autonomic activation and the central processing of sexual incentives in the immediate environ- J. Current Clinical Urology. or reward. This define here as the energizing force that generates includes parasympathetic blood flow to genital our level of sexual interest at any given time. and enables us to breathing rate. LLC 2011 . increased of sexual arousal and desire.

and endocannabinoids (CBs) that shut down ence. provide a sense of pleasure and ecstasy.1  Hypothetical relationship between experi. Opioids released at orgasm nal incentives on libido. (a) inhibits hypothalamic and limbic centers involved in Excitatory systems involve the activation of sexual sexual arousability and attention during periods of arousability by norepinephrine (NE) and oxytocin (OT). Opioids serve a paradoxical dual function that vides moment-to-moment modulation of libido. thalamic and limbic structures that focus attention Blunting overactive serotonergic or endocannabinoid toward particular sexual incentives. attention. Attentional mechanisms involve both hypo. Endocannabinoids activate strengthen or reduce responding. arousability. Note that excitatory and inhibi.. (5-HT). Serotonin acti- tory feedback can occur anywhere in this flow chart to vates mechanisms of satiety. and excitatory systems during normal periods of refractori- stimulus processing from genital sensations and exter.g. but blunting them under normal circumstances can orgasm).Fig. intense sexual reward (e. parasympathetic and sympathetic arousal. Such feedback pro. orgasm). systems can release sexual arousal and desire from tems involve the general activation of opioids.  3. serotonin inhibition . and tion. sedation. blunt sexual reward and subsequent sexual desire. blunting opioid systems when control of autonomic outflow (directing genital blood they are overactivated by stressors can facilitate copula- flow. Sexual arousability involves activation by sexual incentives induces a greater focus- both central and peripheral mechanisms involved in the ing of attention. Thus. hormonal activation. ness. (b) Inhibitory sys. but also to sensi- and attention toward sexual stimuli by dopamine (DA) tize mesolimbic dopamine systems such that subsequent and melanocortins (MC). or when under stress.

and amygdala [13–18]. [1].. far less is known about the activation of libido. PDE-5 inhibitors such as sildenafil. Studies of the melanocortin ago. hypothal- (e. Treatments that enhance penile erection in uli [17. loxan. a region previously implicated in penile erection in gonadally-intact male rats [6. claustrum. dopamine receptor tions such as acute exercise or exposure to stimuli antagonists. females. melanocortin agonists such film [15. 17. inferolateral prefrontal cortex. and may increase libido if anterior cingulate and medial prefrontal cortex. such as nitroglycerine. this does either positron emission tomography (PET) or not translate into an increase in subjective sex. However. ventral striatum/nucleus accumbens. in the mPOA [11]. The ease Vaginal/clitoral arousal: Relative to our under- with which men achieve or maintain erection in standing of the mechanisms underlying penile response to erotic cues can be taken as an index of erection. and imi- with subjective sexual arousal [16]. whereas activation of parietal as PT-141. prostaglandin E1. bremelanotide (formerly PT-141) found that appears to be critical for vaginal blood flow. ual arousal. morphine can induce erectile responses in male hypothalamus. 18]. apo- A subset of those regions (nucleus accumbens. Activation of inferior extrastriate nonhypogonadal men with erectile dysfunction cortex. and linsidomine) also enhance rontal cortex. hypothalamus.g. and midbrain was correlated with subjec- fil. and vardenafil. neutral odors paired with sexual reward [20]. could exert actions centrally. oxytocin. These studies have found common regions of thetic outflow appears to make individuals more activation in men and women. although some of the drugs. In fact. general stimulation of sympa.3  Physiology of Libido 27 anticipation of sexual activity. sodium play an abnormal activation of medial orbitof- nitroprusside. dopamine receptor agonists tive sexual arousal in men following an erotic such as apomorphine. Conversely. In women. although vaginal pulse amplitude in Brain activation during the presentation of response to visual erotica can be increased fol. nearly identical regions of the brain vous system. includ- apomorphine. the inhibitory control of motivated behavior. along with vaginal smooth muscle relax- tions in rats can be provoked by exposure to sexu. However. oxytocin. e. However. ation [21]. “Noncontact” erec. In male and their erectogenic actions in the autonomic ner- female rats. It is presumed that these compounds exert relative to control subjects [19]. and latency to. situa. functional magnetic resonance imaging (fMRI). amygdala) activated by exposure rats following infusions to the medial preoptic of male rats to sexually arousing estrous odors or area (mPOA) of the anterior hypothalamus [8]. or ephedrine [5]. although Penile erection: Erection is stimulated in hypogo- the two latter structures are activated more in nadal men or castrated male rats by androgens men than women viewing the same sexual stim- [6]. reduce both that arouse a sympathetic response can produce physiological and subjective sexual arousal in men increases in physiological sexual arousal. idazoxan. as it it induced erections in healthy men. or to augment by drugs that stimulate nitric oxide release in the genital responses during the presentation of paraventricular hypothalamus or dopamine release visual sexual stimuli. tadala- amus. studies testing the efficacy ally receptive females or vaginal estrous secretions of PDE5 inhibitors to increase vaginal blood flow [10]. and enhanced is for penile blood flow. and inhibit erections in male rats [12]. and vasodilators that act through nitric men with hypoactive sexual desire disorder dis- oxide substrates. 18]. full erection physiologic or psychogenic sexual arousal in can be measured. visual sexual stimuli has been studied using lowing exercise [4]. 7]. have generated conflicting . including the aroused in general. are activated by copulatory stimulation. nists. The nitric oxide-cyclic GMP pathway nist. activity. Such erections are potentiated by androgens. such as haloperidol. and duration of. or pulse amplitude on their own. Thus. and the a2 receptor ago- ing ejaculation and vaginocervical stimulation. the situation contains appropriate sexual cues. a2 receptor cortex in men by erotic pictures was correlated agonists such as yohimbine.g.. Psychogenic erections can be stimulated in men by exposure to visual sexual stimuli. Treatment with andro- erection in response to visual sexual stimuli in men gens facilitates vaginal nitric oxide synthase with erectile dysfunction [9].

desire as it is in females primed with estrogen alone. or that cally or recurrently deficient or absent. odor) is paired with sexual reward. Finally. In preliminary studies. We have shown that presentation of the conditioned stimulus alone induces anticipatory psychomotor stimula- tion and activates brain regions in male and Sexual Desire female rats associated with incentive motivation and attention (e. baso­lateral except that inferred from the definition of and medial amygdala). a significant posi.” the activation of Desire can be inferred in animals by their these two neurochemical systems in the brain willingness to work for sexual reinforcers. sions of amphetamine to the nucleus accumbens sure to different types of sexual stimuli. Recently. To the expressed physically in conscious. afferents to the nucleus accumbens) decrease ological and subjective responses. to increases systems. we have of desire for. Indeed.. in which “desire occur in control animals that receive either no for and fantasy about sexual activity are chroni. increases in male rats in response to jective arousal [22]. and . expo.28 J. indicating that systems psychological interest in sex and behaviors that for sex and reproduction are being activated reflect such interest. or in may form an important part of the pathway that behavior that reflects the anticipation of sexual mediates libido [33]. with desire constituting a and females. association of the odor with reward. Pfaus results. or estrogen alone [32]. despite being given apomorphine. as parts of one another.G. 26]. almond tested. from no appreciable effects. analogies of “sexual desire. and reproductive pro- Hypoactive Sexual Desire Disorder in the cesses (supraoptic and paraventricular nucleus Diagnostic and Statistical Manual of Mental of the hypothalamus). sexual behavior (mPOA. Interestingly. and dopamine subjective arousal and perception of genital receptor antagonists injected peripherally or arousal in women with arousal disorder and centrally to these regions disrupts anticipatory lower vaginal pulse amplitude [23]. Part of the conditioned excitement [29]. most closely resembles the “lust” of patory psychomotor stimulation in male rats are libido. Such activation does not Disorders (DSM-IV-TR) [24]. found selective activation of both oxytocin. desire may bremelanotide increases rates of solicitation in be informed or confirmed by the presence of female rats primed with estrogen and progester- autonomic or central arousal. the melanocortin agonist and arousal are separate processes.. goal-directed extent that solicitation in female rats and antici- behavior. This decrease can be reversed by infu- placement of a vaginal plethysmograph. Several lines of evidence link the increases both dopamine and melanocortin syn- desire for sex to the activation of brain dopamine thesis in hypothalamic and limbic structures. Thus. accumbens. This may operant responding for secondary sexual rein- reflect several variables. sexual desire would be the presence reward and nonreward [31].” By con. women and men regard sexual desire and arousal we found that the dopamine receptor agonist. to increases in genital dopamine release in the mPOA and nucleus arousal without corresponding increases in sub. both conditioned and unconditioned incentive tive effect of sildenafil was shown on both cues that predict sexual reward [28]. many one. respectively. and fantasy about. Microdialysis studies have shown that in subjective arousal. Conditioned partner preferences in rats phase of the ovulatory cycle in which women are occur when a neutral stimulus (e. estradiol activity [27].g. Lesions of the problem conducting studies of female arousal basolateral amygdala (a region that sends glutamate concerns the high degree of variability in physi. Despite the fact that desire selectively. receive random association of the odor with verse logic. including differences in forcers. ventral No agreed-upon definition of sexual desire exists tegmentum). In fact. also increases rates of solicitation distinct definitions [25.g.and Desire can be viewed as distinct from arousal in GnRH-containing neurons by the odor in males animals and humans. nucleus accumbens. sexual activity. and the [30].

and opioid agonists reward is inferred in animals by the strength of infused directly into the mPOA have similar operant or instrumental responding toward a par. Polygamous males. tioned partner preference. male and female rats can be conditioned interest in chasing females. may be primed by treatment with dopamine receptor antagonists do the activation of these two systems by steroid not block the induction of sexual CPP or condi- hormones. Interestingly. bonding in male Prairie voles is disrupted by ciated with reward. If one distinctive Activation of oxytocin and vasopressin path- side of a CPP apparatus is paired with a reward. Sexual male and female rats [41]. are also important components of absolute refractory period. Lesion useful in delineating the behaviors and neuro. nonpaced copulation in females).3  Physiology of Libido 29 androgens activate nitric oxide pathways that the release of endogenous opioids is a critical facilitate dopamine release. Dopamine release ticular sexual reinforcer. copulation but not ejaculation in life and share parental duties [44]. activates (or sensitizes) desire. during Prairie voles have a greater density of the vaso- rewarded training trials blocks the induction of pressin type 1a receptor in the ventral pallidum sexual CPP in both males and females.g. Prairie voles bond with their first sex partner for rience (e. and that it of ovulation [34]. nor do rats. and the other distinctive nent of future social bonding. ejaculation is critical lateral hypothalamus plays an inhibitory role in in the formation of CPP. both Montaine voles do not. naloxone. and in the strength of decreases abruptly in the nucleus accumbens and copulatory responding (i. indicating that dop- amine activation is not a necessary component of sexual reward [38–40]. Contextual factors. such tive salience of females is diminished during the as settings.. For male rats. and viral naloxone blocks the formation of conditioned gene transfection of the V1a receptor to the ven- partner preferences in rats [37. As noted rats lose interest in solicitation and male rats lose above. by injections of an oxytocin antagonist.. Systemic administration of injections of a vasopressin antagonist [45]. and sex. although it is required for animals to display conditioned appetitive Sexual Reward responses and may be necessary for smaller. inhibitory effects in male rats. from behaviors that mPOA when male rats ejaculate and the incen- typically denote desire). The decrease in dop- positive sexual experiences for both men and amine release in the nucleus accumbens may be women. tory sexual activity in males. whereas for female rats sexual arousal. whereas indicating a preference for contextual cues asso. 36]. more appetitive types of reward when animals An emerging idea from animal studies is that attempt to gain access to sex partners and solicit desire is linked to an expectation of reward. copulation (pacing) is critical. studies suggest that the nucleus accumbens plays chemical systems necessary for sexual reward in an excitatory role in sexual arousal whereas the rats [35. ways by sexual reward may be a critical compo- ing sexual experience. This suggests that to display a partner preference based on odors or . 38] and produces tral pallidum of male Montaine voles renders a state of sexual nonreward that makes female them behaviorally monogamous [46]. Monogamous side is paired with a less rewarding sexual expe. The increase in factor in the sexual reward induced by ejacula- female-initiated sexual activity around the time tion in males and pacing in females. Recent work using the conditioned place due to an activation of serotonin release in the preference (CPP) paradigm has been particularly lateral hypothalamus by ejaculation [42]. Systemic administration of opioid agonists that such expectation fluctuates in time given the disrupt the initiation of sexual behavior in both actual level of reward experienced.e. compared to male Montaine voles. Likewise. Monogamous male and female rats will spend significantly bonding in female Prairie voles can be disrupted more time in the side associated with reward. but an excitatory role in the regu- the ability to control the initiation and rate of lation of ejaculation [43]. and the increase in anticipa. Male the opioid receptor antagonist.

30 J.G. Pfaus

other cues associated with sexual reward [47, 48], the activation of inhibitory pathways for sexual
and we have recently found that such cues activate arousal and desire generates a state of reduced
oxytocin and vasopressin neurons, in addition to libido (Fig. 3.1b).
dopamine release. Thus, a consequence of early Activation of opioid, serotonin, and endocan-
sexual reward is bonding to cues that predict the nabinoid release during sexual reward is associ-
reward, cues that become highly arousing and ated with an inhibition of ongoing sexual behavior.
desired. In humans, this process may play an This has been studied in male rats following sex-
important role in the formation of preferences for ual exhaustion. Male rats allowed to copulate with
cues that we find attractive at a distance. multiple ejaculations to sexual exhaustion do not
Brain imaging studies have also been con- respond to female solicitations for a period of
ducted in men and women during manual genital 24–72  h. This inhibition can be reversed by the
stimulation to orgasm [49, 50]. In men stimu- 5-HT-1A agonist 8-OH-DPAT (an autoreceptor
lated to ejaculation, PET revealed an increased agonist that inhibits serotonin release), the a2
activation of the cerebellum and midbrain receptor agonist yohimbine, and the opioid recep-
regions, including the ventral tegmental area, tor antagonist naloxone [52]. Thus, blockade of
zona incerta, and subparafascicular nucleus, opioid or serotonin transmission, or activation of
along with the intralaminar thalamus, lateral parasympathetic pathways involved in erection,
putamen and claustrum. No increased activation can overcome the state of inhibition induced by
was observed in hypothalamic regions, and sexual exhaustion. Activation of opioid transmis-
decreased activation was observed in the sion by stress may also play a role in sexual inhi-
amygdala and surrounding entorhinal cortex. bition. Male rats find novel environments stressful.
Most of these regions are activated by ejacula- In fact, males that are not desensitized to the envi-
tion in male rats, although the general activation ronment in which they have their first sexual
patterns offered by PET do not have the fine- experiences often do not copulate. Preexposure to
grained spatial resolution of the neuronal markers the environment, or treatment with naloxone,
typically used in rat brain sections (e.g., induction increases the proportion of males that copulate on
of nuclear Fos protein). It is possible that small their first trial [53]. Interestingly, sexually naïve
hypothalamic regions may still have been activated males sensitized to amphetamine do not show
but undetected. In women with complete spinal inhibition during their first exposure to females in
cord injury, but that still experienced orgasm a novel environment, despite the drug exposure
from masturbation, fMRI revealed an activation happening weeks before [54]. Although sexually
of hypothalamic structures, including the para- experienced males show signs of fear (e.g., freez-
ventricular nucleus, the medial amygdala, anterior ing) in novel environments, they do not show sub-
cingulate, frontal, parietal, and insular cortices, sequent sexual inhibition if a receptive female is
and cerebellum, by orgasm. Because of the spinal placed into the environment. Together, these data
damage, it was concluded that the stimulation of suggest that sensitized dopamine systems, pro-
orgasm traveled through the Vagus nerve to acti- duced either by sexual experience or amphetamine
vate the brain. preexposure, or blockade of opioid transmission,
can overcome the stress-induced inhibition of
sexual responding in males.

Sexual Inhibition

Sexual inhibition can be induced by stressful life Conclusions
events or following high sexual rewards (i.e.,
during a refractory period in which reproductive Libido reflects our level of sexual interest at any
capacity needs to be regenerated prior to a given time. It is determined that the interaction
resumption of copulation) [51]. In either case, of neural systems underlie sexual arousal, desire,

3  Physiology of Libido 31

reward, and inhibition, processes that are highly References
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Chapter 4
Physiology of Orgasm

Roy J. Levin

Keywords  Orgasm • Cortex • Cerebellum • A number of reviews have been published on
Pelvic musculature • Contraction • Oxytocin the female orgasm [5–13], but fewer on that of
the male [6, 10, 11, 13–15].
The present article summarizes most of the
Introduction known evidence-based facts about human
orgasmic activity with a sprinkle of the salt of
speculation where such facts are still wanting.
The human orgasm, although tantalizingly short,
is perhaps the greatest bodily pleasure that most
men and women can experience without recourse
to drugs. It is a complex of subjective mental Definitions of Orgasm
with physical body changes. Its pleasure can
never be recalled exactly which is perhaps one of It is strangely difficult to define an orgasm accu-
the reasons for desiring its repetition. It dissolves rately despite the fact that most adults have experi-
body boundaries and thus unites lovers in a enced the activity [8]. A review on orgasm published
unique manner. In men, because it normally rou- in 1981 [7] tabled some 13 definitions from the lit-
tinely accompanies ejaculation, it has simply erature, while 20 years later Mah and Binik [10]
been regarded as the drive reward for attempting undertook the same exercise and now listed twenty
procreation, and in evolutionary terms, as a spur six, despite this they preferred not to produce one
to distribute their genes as widely as possible. In of their own. One difficulty discussed by Levin [8]
women, however, because it is far less easily is that each specialty (physiology, endocrinology,
induced, especially by coital penile thrusting brain imagery, and psychology) that examines the
alone, its putative biological purpose(s) have activity has its own requirements for a definition.
been subjected to extensive discussion. This has Another problem arises in ascertaining exactly
resulted in the unresolved dichotomy of whether when an orgasm starts; is it when the subject first
it is an evolutionary adaptation or just a by-product. mentally perceives it starting (subjective initiation)
Unfortunately, the arguments from the various or is it when the first physical manifestations of it
protagonists have become more philosophical appear (objective initiation) as these two may not
rather than physiologically based, have produced occur at the same time. Some physical manifesta-
more heat than light, and will not be repeated. tions have been used to identify the occurrence of
orgasm in females (see Section below on objective
signs of orgasm in women).
Because we do not have the exact picture of
R.J. Levin (*)
the neural brain activity underlying an orgasm,
Sexual Physiology Laboratory, Porterbrook Clinic, most definitions relay on describing the observ-
Sheffield S11 9BF, Yorkshire, England able or reported physical changes. Despite this, a

J.P. Mulhall et al. (eds.), Cancer and Sexual Health, Current Clinical Urology, 35
DOI 10.1007/978-1-60761-916-1_4, © Springer Science+Business Media, LLC 2011

36 R.J. Levin

reasonably comprehensive operational definition identical. More recently, Mah and Binik [17]
for women is “An orgasm in the human female developed and evaluated an orgasm rating scale
is a variable, transient peak sensation of intense (ORS) for assessing sensory, cognitive, and
pleasure creating an altered state of consciousness affective aspects of the experience in both men
usually accompanied by involuntary rhythmic and women. The only substantive gender differ-
contractions of the pelvic striated circumvaginal ence observed in their ORS evaluation was that
musculature, often with concomitant uterine men gave a higher rating to “shooting sensa-
and anal contractions and myotonia, that resolves tions,” which was interpreted as related to the
the sexually-induced vasocongestion (sometimes ejaculation of the semen, a feature of orgasm
only partially), usually with an induction of obviously not well developed for most women.
well-being and contentment” [12]. In the case
of males, “An orgasm in the human male is a
transient peak sensation of intense pleasure cre- Cardiovascular Phenomenon
ating an altered state of consciousness usually
accompanied by involuntary rhythmic contrac-
At the initiation of orgasm, both males and
tions of the pelvic striated musculature normally
females have their highest blood pressure, heart
forcefully ejecting semen, often with concomi-
rate, and respiratory rates of their sexual encoun-
tant anal contractions and myotonia ending usu-
ter ([6], p 278).
ally with feelings of languor, well-being and

Pelvic Musculature Contractions
Common Features of Orgasm
in Males and Females Powerful and highly pleasurable pulsatile con-
tractions of the striated musculature of the pelvis
(especially the bulbocavernosus and ischiocaver-
Despite the fact that orgasm has a strong
nosus) take place at the initiation and during
­subjective component, there are some common
orgasm in men and in most women. In the case
response patterns in men and women, which are
of men, the contractions create the spurting, pro-
described briefly below.
jectile ejection of the semen that is preloaded
into the urethra by the contractions of the smooth
muscle of the vas deferens and capsules of the
Mental Experience prostate and seminal vesicles. Usually, up to six
or seven forceful contractions are needed to
Trying to describe an orgasm in words, either for expel all the semen containing sperm, but a sig-
men or women, is a difficult task especially if nificant number of further contractions can still
there is a loss of conscious focus, yet these needs occur without any fluid expulsion [18], presum-
to be undertaken if we wish to compare mental ably a built-in safety factor to ensure that all the
and physical experiences between the sexes. One sperm are ejected.
ingenious study [16] obtained written descrip- The role of these pelvic muscular contrac-
tions of orgasms from 29 male and 29 female tions in the female is more problematic. Some
subjects and then removed or altered any feature authors regard orgasm as a “sensory-motor reflex
that could identify the sex from which the loop” and that orgasm occurs as a muscular
description came. These were then given to a response, “without the contractions there has
panel of expert judges who had to decide what been no orgasm” [19]. Others do not agree,
sex the descriptions were from. They were not reporting women who have orgasms but do not
able to select them into such groups suggesting perceive any such contractions. Whether this is
strongly that what males and females experience because they are very weak contractions or that
during orgasm is probably very similar if not the women are poor at sensing such changes in

4  Physiology of Orgasm 37

their bodies is not known as there have been no using regional Cerebral Blood Flow (rCBF), and
laboratory studies undertaken on such women. a few of these studies have also examined
A number of functions have been suggested, which orgasm. While they have opened up a completely
are listed below and brief criticisms of the pro- new way to compare what happens in the brains
posals are given in the brackets after each item: of men and women during arousal, it could be
said that in some ways they have created more
1. To eject paraurethral glandular secretions
problems than they have solved. This is because
from the urethra (not all women have these).
the various groups have used different methods
2. To empty the vasocongested genital tissues
of stimulation, different controls for basal val-
(a single orgasm usually does not accomplish
ues, different techniques of handling the data
this, [20]).
obtained, and different interpretations of the final
3. To end sexual arousal (women are serially
results. There is no consensus or clear picture of
brain functioning during sexual arousal and
4. To stimulate male arousal to capture his semen
orgasm. One thing that the studies have accom-
(not all women have the contractions).
plished, however, is the rejection of the concept
5. To create pleasurable feelings (voluntary con-
of an orgasm center in the brain. All the studies
traction of the muscles does not create pleasure).
show that a number of areas of the brain are acti-
Some authors, however, think that they are vated and others deactivated at arousal and
vestigial or an accidental by-product – the prob- orgasm, indicating the concept of a common
able result of the common fetal origins of the multiple site coactivation or a neural network as
striated pelvic muscles essential for male ejacu- a model for brain orgasm [15]. What we don’t
lation, but not for female’s. They are an example understand is how the activated and deactivated
of a “biological spandrel” [21]; as they cause no components combine to create an orgasm; unfor-
harm, there is no reason to actively dispense with tunately while knowing the parts involved is
them and so they remain in the female. obviously essential, we cannot reverse engineer
Bohlen et al. [22] recorded the pelvic contrac- an orgasm from them.
tions in 11 nulliparous women during their According to Georgiadis et al. [23], common
orgasms. They did not find any relation between areas of brain activation at orgasm in men and
the number or strength of the contractions and women are found in the anterior lobe of the cer-
the subjective pleasure of the orgasm. ebeller vermis and deep cerebellar nuclei and
profound deactivations are found in the left ven-
tromedial and orbitofrontal cortex. The only
Rectal Sphincter Contractions prominent difference during orgasm between the
genders was a male-based activation of the peri-
aqueductal gray matter, while in the case of
Rectal sphincter contractions can occur during
women a larger activation of the right insula was
orgasm in some but not all women ([6], p 129) and
observed compared to men, a difference, how-
in males during ejaculation and orgasm ([6], p 174).
ever, mainly caused by the deactivation in men.

Activation or Deactivation of Areas
in the Brain Facial Grimacing

In the last few years, a number of studies have A characteristic face usually occurs in both men
been undertaken using brain imaging with either and women during orgasm. The mouth is held
PET (Positron Emission Tomography) or fMRI open (possibly due to spastic contractions of the
(functional Magnetic Resonance Imaging) tech- surrounding muscles), the eyes are shut, and the
niques during sexual arousal to examine what facial muscles create a grimace that leads to any
areas of the brain are activated or deactivated observer thinking that the person is suffering from

38 R.J. Levin

significant pain rather than exquisite pleasure! was a hormonal mechanism that terminated sexual
The “grimace and contortion of a woman’s face arousal, but later studies showed that this was not
graphically express the increment of myotonic the case in either males or females [27, 28].
tension throughout her entire body” ([6], p 128). While it is known that oxytocin is also
released at orgasm in both men and women, the
actual physiological functions of the nonapep-
Hyperventilation tide have been poorly investigated. Proposals
from animal studies that it is involved in sperm
transport, namely facilitating ejaculation in
Hyperventilation occurs during high levels of
males, uterine contractions in females, and in
sexual arousal and it runs through orgasm. Peak
possible pair-bonding, are still unsettled [27].
respiratory rates as high as 40 per minute have
been recorded ([6], p 277) compared with the
basal levels of 12–14 per minute. The open-
mouthed hyperventilation can be linked to facial Differences Between Female
grimacing (see above) and to vocalizations (see and Male Orgasms
below). It has been suggested that the hyperven-
tilation by lowering the CO2 in the plasma could While there are common features between female
create giddiness and light headedness often asso- and male orgasms as listed above, there are also a
ciated with high levels of arousal and orgasm few differences [29]. In brief, these are:
[24, 25].
1. Unlike males, females generally do not have a
PERT after their orgasms being multiorgas-
Vocalizations mic (but see Section below of female orgasms
with urethral emission).
2. The pleasure of subsequent female orgasms
During orgasm, most males and females vocalize after the first can be better, this is not the case
involuntary, usually nonverbally, and these vocal- for male orgasms.
izations often accompany each pelvic contraction 3. The orgasm of females can be interrupted by
(see above Section on “Pelvic Musculature”). external environmental stimuli or by cessa-
These vocalizations, especially of the female who tion of the inducing sexual stimuli, but once
are said to produce more sounds than males dur- the feeling of “ejaculatory inevitability” is
ing coitus, convey to the sexual partner the fact experienced by a male, the ejaculation and
that they are experiencing an orgasm of ecstasy concomitant orgasm is inevitable.
and extreme pleasure. They are much appreciated 4. One type of recorded anal contraction at orgasm
by males who are often taking the lead in sexu- in males has not been observed in females
ally arousing the female and like the feedback of (a divided rhythmic pattern), but the number of
their successful lovemaking [26]. The vocaliza- recordings for both sexes is very small [22].
tions, moreover, act as a sexual stimulus, espe-
cially to the male, enhancing his arousal. There are also some claimed differences in
brain activation at orgasm [15].

Release of Prolactin and Oxytocin
Female Orgasm
Prolactin is released in both sexes at orgasm
significantly increasing the concentration of the Sexual arousal of the female to induce orgasm is
polypeptide in the plasma for approximately 60 min usually accomplished by stimulation of the gen-
after the orgasm. It was initially proposed that this italia (clitoris, labia minora, vagina especially

4  Physiology of Orgasm 39

the anterior wall) and the surrounding area The duration of orgasm has been measured
(perineum, anus, inner thighs) facilitated by in the laboratory. Based on 26 healthy young
nipple/breast stimulation [30, 31]. In some sen- subjects indicating the start and end of their
sitive women, orgasm can be induced by mental felt orgasms, Levin and Wagner [35] recorded
imagery alone [32], while other unusual activa- their duration as 19.9 ± 12  s (Mean ± Standard
tions in aroused women have occurred from Deviation). The measured durations were not
brushing their eyebrows or pressure on their significantly correlated with their subjective
teeth ([5], p 590). Laboratory studies with spi- grading. When the subjects tried to estimate
nalized women have indicated that vibration of the duration of their orgasm immediately after,
the cervix can lead to orgasm via a vagal path- the estimates were nearly half of their measured
way bypassing the spinal cord [33]; whether this ones, indicating that orgasm creates an alteration
path is in operation in able-bodied women has of a subject’s personal time sense. Clearly, simply
not yet been established. Consciousness is not asking women about their orgasm duration does
required because orgasm can occur even during not give a valid “objective” duration.
sleep. It is often assumed that for the female In relation to the intensity of orgasm, this has
orgasm to occur, the willingness of the female to been correlated with: (1) the increase in heart
accept the sexual stimulation is an essential fac- rate at orgasm, the greater the increase the more
tor. However, unsolicited or nonconsensual intense and pleasurable was the orgasm [36]
stimulation can lead to unwanted sexual arousal confirmed by Alzate et  al. [37]; (2) the more
and even orgasm [34]. women were in love/emotionally close to their
According to the account of Masters and partner, the more they were satisfied with the
Johnson ([6], p 135), the female orgasm starts quality of their partnered-orgasms [38].
psychologically with a very brief transient sen-
sation of “stoppage” or “suspension,” which is
followed by an intense thrust of clitoral aware- Uterine Contractions
ness that radiates into the pelvis. A suffusion of
pelvic warmth occurs which spreads into the rest Masters and Johnson ([6], p 116) reported that
of the body. The physiological start of the orgasm specific uterine contraction patterns do not
(p 128) occurs with intense pleasurable pulsing develop unless orgasm is occurring and that
sensations perceived concomitant with contrac- when this occurs the degree of contraction paral-
tions of the uterus, pelvic musculature, vagina, lels the intensity of the orgasm. The types of pat-
and anus. Involuntary vocalizations often accom- terns, however, were not described and no data
pany contractions of the latter three [26]. When was presented to support these conclusions.
these contractions have died away, most women Unfortunately, remarkably few records of uter-
are left with a feeling of calm, lassitude, and ine contractions at orgasm have been published
­satisfaction and often with a dissipation of their and the importance of these contractions to the
sexual tensions. The dissipation of the vasocon- development of the subjective feeling of pleasure
gestion in the vagina, however, is often only from the orgasm is poorly characterized. Indeed,
­partially complete [20]. This may be part of the exact mechanism of the induction of the uter-
the  explanation why, unlike men, women can ine contractions has yet to be identified, whether
undertake another orgasm immediately after the from oxytocin release at orgasm or from adren-
previous and some can continue with them with ergic innervation or from both.
appropriate stimulation for a considerable Meston [39] claimed that hysterectomy, while
­number. It is said that nothing is as good the not having a direct effect on sexual function, did
­second time, but this does not apply to women’s in a number of women decrease their orgasmic
orgasms as for many the later ones can be more pleasure which they related to their loss of the
pleasurable. orgasmic uterine contractions.

40 R.J. Levin

Typologies of Female Orgasm periurethral glands. The great variability in these
glands has recently been confirmed with MRI
imaging [44]. The volume ejected has been
There is still controversy over a possible typol-
described as ranging from less than a milliliter to
ogy for the female orgasm. According to Masters
a remarkable, but unconfirmed, 90–900 mL [45].
and Johnson ([6], p 67), orgasms, however and
There is no genital structure that can secrete or
whatever anatomical site they are generated from,
store the latter volumes, such extreme volumes
are physiologically identical, “clitoral and vagi-
have been called “gushing” and is proposed to be
nal orgasms were not separate biologic entities.”
different to the urethral emissions [46].
Other investigators, however [40–42], found that
Women are said to have more intense orgasms
women reported that stimulation of different sites
with ejaculation than those without [47]. The
created different sensory and orgasmic feelings,
suggestion has been made that as the type of
especially in relation to those generated by clito-
female orgasm accompanying this is similar to
ral stimulation compared to those generated by
those in ejaculating males, females having this
anterior vaginal wall stimulation. Stimulating the
orgasm type will likely experience a post ejacu-
clitoris gave “warm, ticklish, electrical, sharp”
latory refractory time (PERT, see section below)
feelings, while stimulating the vagina was “throb-
when they are unable to have another orgasm for
bing, deep, soothing and comfortable” [42].
sometime after (see [48] for references).
Limited physiological evidence is available to
suggest that the balance between uterine smooth
muscle and pelvic striated muscles contractions is
different when orgasms are created either by stim- Objective Signs of Orgasm in Women
ulation of the vaginal anterior wall or by clitoral
stimulation [30]. Singer [43], a philosopher, pro-
Orgasm is a complex of subjective and physical
posed from the limited descriptions in the litera-
events. The latter can either be observed or mea-
ture available to him at the time three types of
sured and they have been used to identify whether
female orgasm which he named (1) vulval, (2)
an orgasm has taken place or not [9]. The changes
uterine, and (3) blended, a mixture of (1) and (2).
induced by orgasm are listed in Table 4.1.
The evidence for this typology was weak relying
on descriptions of orgasms by a female novelist
Table 4.1  Specific objective markers of female orgasm
and experimental descriptions of a single couple
Those indicating impending orgasm (prospective)
during coitus (see [30] for details and criticisms).
Color changes of the labia minora (pink to deep red)
An orgasm typology based on the characteris-
(Masters and Johnson [6])
tics of the pelvic muscular contractions measured
Those occurring during the orgasm (current)
at orgasm was suggested by Bohlen et  al. [22],
Vaginal contractions (induced by rhythmic
but as they only studied 11 women, two of whom pelvic striated muscle contractions) (Masters
had irregular contractions, the attempt was pre- and Johnson [6])
mature and has received no confirmation. Uterine contractions (Masters and Johnson [6])
Anal sphincter contractions (Masters and Johnson [6],
Van Netten et al. [77])
Release of prolactin (Levin [27] for reference)
Female Orgasms with Urethral
Those occurring after orgasm (retrospective)
Emission Areolar decongestion (rapid, causes corrugation of
areolae) (Masters and Johnson [6])
Raised and maintained prolactin levels in the plasma
In a number of women, urethral emissions occur (Levin [27] for reference)
at orgasm and, in popular parlance, this is often Immediate transitory increase in vaginal pulse
called “female ejaculation.” The fluid ejected is amplitude (VPA) (Meston et al. [12], p 793)
claimed not to be urine, but is thought to be Rectal pressure changes (8–13 Hz band): marker for
a secretion from the urethral paraurethral or clitoral-induced orgasms (Van Netten et al. [77])

4  Physiology of Orgasm 41

Specific Brain Activity During allows the semen to enter the distended bulb and
Female Orgasm urethra of the penis. The semen is propelled into
the urethra by the contractions of the smooth
muscles of the ducts and the capsules surround-
There are still very few studies of brain activity ing the accessory organs, but the forceful ejec-
during the female orgasm that by Georgiadis tion of the semen from the penile urethra is by
et al. [49] are the most comprehensive. They used the pulsing contractions of the pelvic muscula-
PET to measure rCBF during orgasm induced by ture, mainly the bulbocavernosus. The first few
clitoral stimulation and compared it with an imi- are powerful and highly pleasurable, and subse-
tation orgasm faked by the subjects. Orgasm was quent ones are less so gradually weakening until
mainly associated with reduction of rCBf in the they die away. Ejaculations without the striated
amygdala and profound reductions in the neocor- pelvic muscle contractions are not as pleasurable
tex, especially in the left lateral orbitofrontal cor- as the semen seeps away. After ejaculation, a
tex, inferior temporal nuclei, and anterior period occurs when the male cannot have either
temporal pole. The deactivation was thought by a repeated erection or an ejaculation [48], this is
the authors to be an indicator of behavioral disin- called the Post Ejaculatory Refractory Time
hibition during orgasm. The deep cerebellar (PERT); it is shorter in young men (minutes) and
nuclei, however, showed increased rCBF pre- increases in duration on aging (hours).
sumed to be involved in the orgasm-specific mus- As in the female, consciousness is not required
cle contractions. An unusual finding was the lack for orgasm as it can occur during sleep (wet
of effect of arousal and orgasm on increasing the dreams or nocturnal emissions) and ejaculation
rCBF in the hypothalamus, an area noted for stor- and orgasms can be induced involuntary by
ing and releasing oxytocin and vasopressin at another even if their stimulation is nonconsen-
orgasm. Bianchi-Demicheli and Ortigue [15] sual [34].
have critically reviewed the neural control of the
female orgasm including the role of the brain-
spinal cord integration.
The Male Orgasm with Ejaculation
of semen
The Male Orgasm
Under normal conditions, the male orgasm is
Masters and Johnson [6] characterized the male usually concomitant with ejaculation, but as the
orgasm/ejaculation process into two stages. The two have separate mechanisms [24], it is possible
first (Stage 1) represented the contractions of to have an orgasm without an ejaculation and an
the smooth muscle of the accessory organs start- ejaculation without an orgasm.
ing at the vasa efferentia of the testes, passing
along the epididymis, and then to the vas defer-
ens and seminal vesicles and prostate. Seminal
The Male Orgasm Without
fluids are added to the ejaculate from the testes,
epididymis, seminal vesicles, and prostate. The
Ejaculation of Semen
internal sphincter of the bladder contracts to pre-
vent retrograde entry of the ejaculate into the It is possible for a male to have an orgasm with-
bladder. The sensation of “ejaculatory inevitabil- out the emission of semen. There are a number
ity” (feeling the ejaculate coming) arises just as of conditions when this can take place. Males
Stage 1 is initiated; at this stage, it is not possible suffering from hypogonadism with its concomi-
to prevent ejaculation occurring. tant poor levels of androgens do not manufacture
The second stage (Stage 2) occurs with the significant amounts of semen and thus orgasm
relaxation of the external bladder sphincter that occurs with a “dry ejaculation.” Similarly, males

42 R.J. Levin

who have repeated ejaculations accompanied stimulation” [50]. Other descriptions suggest
with semen discharge in the end exhaust their that penile orgasms have between four and eight
seminal fluids and thus have orgasms without contractions, while those from the prostate
any semen being ejaculated. It is also possible around 12. Perry [51] characterized them as
for the semen to be moved retrogradely into “emission type reflexive orgasms” with occa-
the bladder so that no semen appears during the sional oozing of semen from the penis and
ejaculation. The urine, on urination after such a reported that they can be repeated several times
scenario, can appear cloudy/milky because of in a subject. Levin [8] speculated that this type of
the diluted semen. Treatment with a number of activity indicated that only contractions of the
drugs (e.g., alpha blockers) can also prevent the smooth muscle of the genital ducts and capsules
ejaculation of semen, but leaves the orgasm were involved without any of the pelvic striated
intact [18]. muscles as a seeping semen orgasm of weak
intensity occurs in males whose striated muscles
are paralyzed [52].
Orgasms from prostate stimulation were
The Post Ejaculatory Refractory ignored in the studies of Masters and Johnson
Time (PERT) [6], in the popular account of orgasm by Margolis
[11], and even in the extensive review of the sci-
One very highly significant difference between ence of orgasm by Komisaruk et al. [13]. Until
the male and female orgasm is that, in the male critical scientific investigations of these prostate-
after its occurrence with ejaculation, there is a induced orgasms are undertaken in the labora-
period called PERT when neither a second orgasm tory, our knowledge of the activity will remain
nor erection can occur. However, if the sexual anecdotal and speculative.
stimulus is novel or of greater intensity, then a
shorter PERT occurs. The physiological mecha-
nisms underlying this refractory time are poorly
understood [48]. Women do not appear to experi- Specific Brain Activity During Male
ence this feature after orgasm except for the pos- Orgasms
sibility of those “ejaculating” at orgasm [48].
There have been few studies on orgasm and ejac-
ulation in males. Holstege et  al. [53] were the
first to use PET to measure changes in rCBF in
Orgasms Induced by Prostatic
the brain during arousal and orgasm/ejaculation
Massage with the female partners of the males undertak-
ing simulation of the penis. Primary intense acti-
Massaging the prostate via the rectum digitally vation was seen at the mesodiencephalic
or by a physical device can create an orgasm transition zones which includes structures such
without any stimulation of the penis. It is not an as the midline, ventroposterior and intralaminar
activity, however, liked by every male and it is thalamic nuclei, the suprafascicular nucleus, the
said that it takes time and practice to achieve the zona incerta, the lateral segmental central field,
orgasmic status by this type of stimulation. There and the ventral tegmental area. Strong increases
have been no published reports on laboratory were observed in the cerebellum, while decreases
studies of prostate-induced orgasms in compari- were found in the amygdala and adjacent ento-
son with penile-induced orgasms. All the descrip- rhinal cortex. Neocortical activity was only
tions available are anecdotal. It is claimed that found in a few areas exclusively on the right side.
such orgasms are “deeper, more widespread and It is interesting to note that the activated mesodi-
intense and last longer than those from penile encephalic zone contains a dopaminergic group

4  Physiology of Orgasm 43

of neurons that is connected to a large range of Orgasm and Enhancing its Intensity
behaviors that are rewarding. of Pleasure

The experience of orgasm in both men and
women is of course extremely pleasurable, but it
Typology of Male Orgasms
is of great variety. The initial early orgasms that
occur during sexual development are usually far
Most authors assume that there is no typology of less pleasurable than later ones in adulthood.
the male orgasm and that they are all the same. Anecdotal reports of individual’s first orgasms in
However, there is anecdotal evidence that either males or females indicate that they are of
orgasms created by prostate massage are reported poor quality and not very exciting or satisfying,
to be somewhat different from those obtained by and individuals appear to have to “learn” and
penile stimulation (see Section above on orgasms accept the orgasmic pleasure [7]. Fisher [42]
induced by prostatic massage). Zilbergeld [54], a examined many physiological aspects of respon-
clinical psychologist and onetime practicing sex siveness in women, but could not find one that
therapist, claimed that he had orgasms different had any bearing on orgasm consistency. Anyone
to the pattern described by Masters and Johnson who has experienced orgasms, even as an adult,
[6] and that a number of other men told him that knows that some are much more intense and plea-
they also experienced different patterns. This is surable or satisfying than others. The factors that
an unexplored area of male sexuality. influence the intensity of pleasure of an orgasm
are, unfortunately, poorly known. Novelty of the
sexual stimulation is one [5]. Duration between
orgasms is another significant factor especially in
Special Considerations males; after a long period without sexual arousal,
the subsequent orgasm is usually intense. It was
suggested that the cause of this increase in plea-
Can We Tell When Someone
sure was that a larger volume of semen was ejac-
is Faking an Orgasm? ulated ([6], p. 216). Levin [56], however, reported
on a number of studies indicating that this rela-
Faking an orgasm by the male when the penis is tionship between a larger volume and increased
outside the vagina is clearly difficult as in most pleasure does not hold. The duration of arousal is
cases orgasm and the ejaculation of semen nor- also of some benefit; short rapid arousal usually
mally occurs together. Faking a male orgasm leads to a quick and less intense orgasm as
with the penis inside the vagina is easier as the opposed to that brought about by a slow build up
semen is not seen. In a pilot study, heart rate employing teasing, intermittent stimulation.
responses in a male could be used to distinguish Many attempts have been made to try to
between real orgasms with an ejaculation and enhance the intensity of orgasms, but most of
faked orgasms without ejaculation [55]. In the the claims to having achieved this are usually
case of females, not so very long ago the answer anecdotal reports unsupported by any scientific
to the heading question would have been “no we evidence. However, androgens are thought to be of
cannot!” However, there are now measurements importance in both men and women; low levels
that can identify the differences between females usually predicate poor quality orgasms.
having an orgasm and faking one. Georgiadis Exercising the pelvic striated musculature,
et al. [49] found that by examining the frequency namely the bulbocavernosus (bc) and ischiocav-
characteristics of recordings of the contractions ernosus (isc), by contracting them some 60 times
of the rectum, they could easily distinguish 3 times a day for about 6 weeks is claimed to
between a real orgasm and a faked one. enhance the pleasure of orgasm both for men and

44 R.J. Levin

for women. Unfortunately, the demands of the Female Orgasm and Reproduction
regime make it rarely maintained (see [57] for
references). According to Berman et  al. [58],
The putative role of the female orgasm in repro-
voluntarily contracting the bc and isc muscles in
duction has been a contentious issue for many
the female contributes and intensifies sexual
years with opposing schools of thought. One group
arousal and orgasm.
argues that orgasm has no scientifically proven
Some recreational (illicit or street) drugs are
function as a reproductive mechanism, while the
claimed to influence the intensity of orgasm.
other supports the concept that the uterine contrac-
Unfortunately, many, if not most, of the studies do
tions induced by orgasm facilitate rapid sperm
not distinguish between the effects during the early
transport from the vagina to the uterus by their
use of the drug and the effects after its chronic use,
“upsucking” action. Unfortunately, the latter pro-
which often leads to a deterioration of all aspects
posal ignores the fact that during high levels of
of the sexual response in both men and women.
sexual arousal the uterus and its cervix is pulled up
The volatile vasodilator amyl nitrite (street
well away from the vaginal pool of semen by the
name “poppers”) was much employed especially
mechanisms of vaginal tenting [6, 65]. Furthermore,
by homosexual males to enhance orgasm through
freshly ejaculated sperm are trapped in the semi-
inhalation when orgasm begins; its action is pos-
nal gel that needs enzymic breakdown; they are
sibly mediated through its transient dropping of
incapable of fertilizing the ovum until they have
the blood pressure, compromising higher brain
been reprogrammed by a complicated process
functions which may be inhibitory to pleasure.
called “capacitation.” This process involves sperm
Anecdotal reports on the injection of heroin claim
interaction with various activating agents in the
it to give a sensation (the “rush”) likened to that
glandular seminal fluids [66], which are only
of an orgasm, but in a study of heroin addicts [59]
brought together at ejaculation [65]. All this takes
feelings of sexual orgasm on injection were rated
a considerable time and so rapid transport of
relatively low down a 20 point feelings scale
sperm is the last feature needed; such transport of
(ninth for males and 15th for females). This may
uncapacitated sperm would serve no functional
be because chronic use of heroin is known to
purpose and they would be wasted as they cannot
impair all phases of the sexual response. However,
fertilize an ovum. In fact, there is now evidence
brain areas that are activated during orgasm also
that sexual arousal in the female creates genital
appear to be activated during the heroin rush [53].
tract conditions that delay sperm transport, thus
A study with 20 male and 15 female “ecstasy”
allowing decoagulation and the precapacitation/
users (MDMA 3,4-methylenedioxymethamphet-
capacitation changes to take place. Strangely, but
amine) reported that the drug delayed their
not unexpectedly given the previous facts, the
orgasms but made it more intense in 85% of the
fastest sperm transport is in the nonsexually
males and 53% of the female [60].
aroused woman (see [65] for references).
Frequent use of cannabis (marijuana) does not
appear to be associated with sexual problems in
females, but in males it is linked with delay or
prevention of orgasms in some men and with pre- Female Orgasm After the Menopause
mature orgasm in others [61]. Johnson et al. [62]
also noticed that cannabis users were more likely A worldwide survey has indicated that sexual
to experience inhibition of orgasm, while Halikas desire and activity are widespread among the
et al. [63] found users showing an increase in the middle-aged and persist even into old age [67].
duration of coitus, but a decrease in the number Sexual dysfunctions, however, do increase with
of orgasms. The use of induced asphyxia to age in females with the advent of the menopause
enhance the pleasure of orgasm (asphyxiophilia) is when estrogen secretion is greatly reduced, but
an extremely dangerous, possible life-threatening especially in males with the reduction in testos-
behavior practiced mainly by males [64]. terone [68].

4  Physiology of Orgasm 45

In their laboratory investigations of human Male Orgasm with Aging
sexual responses, Masters and Johnson ([6], p 223)
compared those in the postmenopausal women
In males after 50, there is a gradual decrease in
with younger premenopausal subjects. They found
the testicular secretion of androgens which
that the former took longer in achieving full tumes-
becomes more severe in some individuals than
cence of the clitoris, had either a decrease in the
others. This decrease leads to sequelae of physi-
normal expansion of their breast volume or it was
cal and metabolic changes now designated as the
absent, and showed a delay or even an absence of
“andropause.” It is claimed that the orgasms in
vaginal lubrication and a decrease in their vaginal
aged men are less easily obtained and are less
expansion (tenting). At orgasm, the postmeno-
intense [71], but there is little published objec-
pausal women had fewer vaginal contractions and
tive evidence [13]. Most discussion relies heav-
rarely showed any rectal/anal sphincter contrac-
ily on the laboratory data obtained by Masters
tions. The latter were regarded as an indicator
and Johnson [6]. They reported on ejaculation/
of the intensity and pleasure felt by subjects during
orgasm in 39 males aged 51–89 years. In these
their orgasm. Because postmenopausal women
men, marked “reduced ejaculatory prowess” was
had few such contractions, it was inferred that
evident as they could not expel the semen as far
there was “a generalized reduction in the intensity
as younger men and the number of their pelvic
of orgasm expression as part of the aging process”
muscular contractions was greatly reduced to
([6], p 229). Unfortunately, this wording is ambig-
one or two at the most, leading to a reduction in
uous and it could mean there was a real decrease in
their “sensual experience” possibly impairing
the felt intensity of the orgasm or that, at specific
the “psychosexual pleasure of the ejaculatory
sites, the physical signs of the orgasm intensity
process,” viz, their orgasms.
were reduced [69]. Basson [70] reported from her
clinical experiences that androgen-deficient post-
menopausal women had difficulty in achieving
orgasm, and when they occurred, they were far Postorgasmic Illness Syndrome
less intense. More recently, even young healthy
premenopausal women reported that the quality of
their orgasms was significantly reduced by the This is a rare syndrome [72] first described in
pharmacological induction of experimental hypog- two patients by Waldinger and Schweitzer [73].
onadism created by injections of depot leuprolide After an ejaculation/orgasm, the patients suffered
acetate for 5 months [68]. from extreme fatigue, a flu-like condition with
Some postmenopausal women experience rhinitis, itching eyes, irritability, and decreased
pain during and after the uterine contractions mood within 20–30 min. These symptoms grad-
induced during orgasm ([6], p 119 and 238). The ually faded away over 3–7 days. The etiology of
pain is possibly caused by the effects of estrogen the condition is unknown and there is no specific
lack created during the postmenopause. The treatment for it.
contractions of the uterus are mediated by both
adrenergic and oxyntergic activation. In the pre-
menopausal woman, these are balanced by the
Do Orgasms have Health Benefits
inhibitory, smooth muscle relaxing effects of the
vipergic innervation of the uterus mediated by Other than Pleasure?
the neurotransmitter VIP (Vasoactive Intestinal
Peptide), but in postmenopausal women VIP is It is fitting to end on the positive health aspects
without action in the low estrogen condition so of having orgasms apart from the pleasure and
that the procontractile innervation is left unop- contentment they can impart. In a review of the
posed and presumably can cause uterine spasm beneficial roles of sexual activity, Levin [28]
and its attendant pain of hypoxia [69]. noted that orgasms have been used to reduce the

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11: Handbook of sexual dysfunctions. 2009. Sex and death: 991–7. 2005. Graziottin A. Rubinow DR. Taylor Segraves R. women share intimate secrets of sexual self-acceptance. Emmaus: Rodale Press. Feeling good is good for men. Gingell C.315: C.34:565–76. Steinberg EM. ology of genital function. p. ual attitudes and behaviours. Women’s sexualities: generations of 70. Oxford: Health Press Ltd. you. 1995. Levin by endogenous molecules. 1997. Schweitzer DH. 71. Plaut SM. Schmidt PJ. and lengthen your life. 217–48. 2002. 2006. Nicolosi A. In: Balon R. BMJ (Clinical Research. 67. 2000. Glasser DB. 8–13 Hz fluctuations in rectal pressure 72. Basson R. Waldinger MD. Pharmacology induced hypogonadism 1641–4. Francis. Georgiadis JR. Sexuality and the menopause. 1999. Van Netten JJ.28: dysfunctions after age 40: the global study of sex. Urology. Yarnell JD. .279–85. Levin RJ. Oakland: New Harbinger. 4:23–31. The impact of the menopause on the physi.(Suppl):10–5.48 R. Florida: Taylor & 1636–45. Arch Sex Behav. 2001. 2004. Ellison CR. how pleasure can boost your immune system 69. Heaton JWP. Waldinger MD.64: 74. Laumann EO. are an objective marker of clitorally induced orgasm ders. Male ejaculation and orgasmic disor. ed). Postorgasmic illness ED. Front Biosci. Moreira 73. 77. J SOGC. are they related? Findings from the Caerphilly cohort 68. 2008. 251–5. Kortekaas R. function. Menopause Rev. editors. Brennan FX. Sexual dys. in women.J. 2004. 76. Frankel S. J Sex Marital Ther. Negro PP. Neuropsychopharmacology. Davy Smith G. Charnetski CJ. Haq N. Nieuwenburg A. Gibson study. Paik A. Sexual behaviour and sexual syndrome: two cases. and sexual function in healthy young women and 75.

J Sex Med.111/j.2010. The effectiveness of the treatment and that the bulk of the evidence indicated that the ­suggested that the mechanism(s) underlying female orgasm has little or no effective role in the POIS may be an autoimmunogenetic/allergic transport of spermatozoa in natural human coitus condition.1743-6109. Waldinger M. Postorgasmic illness syndrome (POIS) Postorgasmic Illness Syndrome in 45Dutch Caucasian males: Clinical char­acteristics and evidence for an immunogenic patho­genesis (Part 1). 31 months in another. Can the controversy about the putative role of the human female orgasm in sperm transport be settled with our current physiological knowledge of coitus? J Sex Med.1743-6109.2012002162. Zwinderman AH. 49 . References Waldinger MD. In a further study 2 patients diagnosed with POIS agreed to a desensitisation pro- In relation to the putative role of the female orgasm gramme  using their own semen. Zwinderman & Schweitzer (2011) to ­illness syndrome (POIS Part 2). During the programme taken to support the concept. J Sex Med. The conclusion was there was gradual amelioration in the symptoms that there was no experimental study able to of POIS of 60% in the former case and 90% in unequivocally confirm the proposed mechanism the latter.2010.Addendum Since the chapter was written a number of papers immunogenic etiology.02166. doi. doi. Meinardi MM. Some 33 men diagnosed have been published that add additional findings with POIS were examined using a skin prick to topics dealt with in the review chapter. Meinardi MM. 2011.111/j. Caucasian males: beneficial effects in postorgasmic Meinardi. 2011.10.10.x. Schweitzer DH.x.x. Schweitzer DH.1743-6109. 2011. This results suggested that POIS could be due to a Type 1 and Type 1V allergy to the male’s own Female Orgasm and Reproduction semen. Hyposen­ sitization therapy with autologous semen in two Dutch drome (POIS) have been conducted by Waldinger. investigate whether the condition could have an doi.10. test  with autologous diluted seminal fluid. injecting initially very diluted seminal fluid port of sperm through the female reproductive ­subcutaneously (of gradually increased concen- tract the recent review by Levin (2011) examined tration) ending over 15 months in one case and in critical detail the experimental studies under. of these 29 (88%) showed a positive test.111/j.02167. This involved and its release of oxytocin in facilitating the trans. Levin RJ. Further study of the postorgasmic illness syn.

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Introduction emotional. there is only limited attention given to their sexual social class. Goldstein (*) during medical school training. it is important that providers of such female • Neurotransmitters • Androgens • Hormones oncologic health care be familiar with the basic aspects of appropriate women’s sexual health. ing. residency train- Sexual Medicine. less of sex. age. CA. Mulhall et al. logic patients will be highly associated with their the sexual rights of all women must be respected. discrimination. race. and violence. 51 DOI 10. and fulfilled. cases. © Springer Science+Business Media. Partner’s concerns. psychological. mental. the sexual health problems of these onco- For sexual health to be attained and maintained. a satisfying sex life may be oncologic disorders who also have sexual health important throughout their lives [23–26]. religion. USA Furthermore. San Diego. Current Clinical Urology. while freedom from all forms of discrimination regard- great attention is provided to the oncologic concern. secondary to CA. “Sexual health” refers to a state of physical. ally complex and are. Women who have oncologic disorders Women’s sexual problems may be associated also have the right to sexual pleasure. Women who have onco- the treatments for their oncologic condition [8–12]. a intellectual. sexual with significant personal distress including pleasure is a source of physical. and spiritual well-being [27]. sexual medicine issues are usu- and University of California at San Diego. To pro- egies to effectively manage their sexual health vide the best overall women’s oncologic health concerns. however. logic disorders have the right to sexual equity: the In the vast majority of cases. Cancer and Sexual Health.1007/978-1-60761-916-1_5. have sexual health concerns [1–7]. and relationship issues J. Oncologic health care clinicians often have received limited training in the diagnosis and treatment of women with sexual health concerns I. disability. engaging female patients presenting with primary In some women. physiologic. USA psychologic. Alvarado Hospital. San Diego. a diminution of self-worth and self-esteem. in general. LLC 2011 . sexual orientation. and emotional health problems.P. or physical. reduction in life satisfaction. and a decline in the Multiple challenges are commonly faced while quality of her relationship with her partner [13–22].Chapter 5 Physiology of Female Genital Sexual Arousal Irwin Goldstein and Jonathan Silberstein Keywords  Arousal • Engorgement • Lubrication care. and/or subspecialty training [28–31]. gender.). office will include women patients who may also to have pleasurable and safe sexual experiences. In many free of coercion. female oncologic health care problems and/or protected. It is simply difficult to find the time and sexual health may also be impaired and this may the opportunity to discuss with such patients strat- further adversely affect the relationship. and social well-being related to sexuality. (eds. Women who have oncologic disor- ders have the right to a positive and respectful The waiting room of a busy oncology practitioner’s approach to sexuality and to sexual relationships.

may wish to become members of the International evidence-based. There are five regions of regulating genital physiological responses by The International Society for Sexual Medicine. basic science and clinical infor. biologic-based female sexual academic. ture that adversely affect the response to physi- order. There are many psychologic tile dysfunction. with sexual arousal concerns that appear biologi- ner’s sexual health [92–99]. endometriosis. Interested healthcare pro- Various biochemical factors modulate the fessionals should visit the organization’s Web site. pelvic nerve stimulation [112–115]. vasocongestion. hysterectomy. urinary incontinence.52 I. menopause. clinical. molded with distinct couple dynamics. tides (such as neuropeptide Y) also modify genital ety. pregnancy and childbirth. his sexual the oncology practitioner. anxi. that is. sexual pain disorders. and practitioners about women’s sexual health. hypothyroid.isswsh. pelvic associated with genital tissue alterations in struc- floor dysfunction. and/or interpersonal tion and vascular and nonvascular smooth muscle relationship issues [32–42]. Various hormonal factors modulate the female bladder cancer. and to Genital sexual arousal is mediated by a host of provide the public with accurate information about neurotransmitters and vasoactive agents. metabolic syndrome. Female sexual arousal responses are mul. infertility issues. distraction. Goldstein and J. uterine fibroids. stand physiologic. interstitial estrogens and androgens that happen in meno- cystitis. throbbing. components that occur following sexual stimula. The objective of want to improve their clinical management skills this chapter. and scientific organization. Biologic factors cell contractility [105–111]. female genital sexual arousal response. and clinical prac- engorgement. Society for the Study of Women’s Sexual Health mation to oncology practitioners to better under. women’s sexual health. should the male physiological and molecular basis of female geni- partner experience premature ejaculation. an international. tissue structure and function. and vulvar dermatologic disorders [43–91]. female mones are critical in the maintenance of genital genital mutilation. hyperlipidemia. Lowered levels of estrogens renal failure. purposes of ISSWSH are to provide opportunities tifaceted events consisting of central and genital for communication among scholars. ological modulators. At the discretion of Peyronie’s disease. The goal of this chapter is to provide a multi- Women’s sexual health problems may also stem disciplinary approach to better understanding the from the male partner. education. managing women with sexual dysfunction and be It is important that oncologists who are par- aware that both psychologic and biologic issues ticularly interested in women’s sexual health or cause sexual health problems. the . or prostate cancer. Sex steroid hor- disease. swelling. sionalism in research. erec. sexual neuroses. Silberstein that are interrelated in unique and individual mediating the tone of vascular and nonvascular ways. inability to have an orgasm. (ISSWSH). pause induced by many oncologic treatments are sity. persistent genital arousal dis. tal sexual arousal. and physiologic interactions. Other sexual medicine and nonadrenergic noncholinergic overactive bladder. ­societies such as the International Society for ters (such as nitric oxide) play a critical role in Sexual Medicine. tice relative to women’s sexual health. it is advised that women dysfunction can adversely affect his female part. breast cancer. diabetes mellitus. Lowered levels of ism. In particular. organ prolapse. sleep apnea. rectal cancer. is to provide relevant. multidisciplinary. may involve such pertinent factors as aging. sexually and androgens are also associated with reduced transmitted infections. urinary tract genital blood flow and lubrication in response to infections. sexual inhibi. however. researchers. Vasoactive peptides (such as Psychologic factors include previous sexual vasoactive intestinal polypeptide) and neuropep- trauma and abuse. Adrenergic http://www. psychoses. to tion. obe. and lubrication (wetness) [100–104]. sexual arousal by regulating epithelial cell func- tions or idiosyncrasies. women interpret genital response support the highest standards of ethics and profes- as pulsing. cally focused undergo psychologic management Health care clinicians need to be holistic in concomitant to the biologic-based care [12]. depression. ­coronary artery genital sexual arousal response. The arousal. smooth muscle.

Sexual excitation involves such neurochemi- and production of lubricating fluids (mucus and cals as oxytocin. or receptor binding of vagina. an alpha-1 adrenergic agonist. Factors that Pacific Society for Sexual Medicine. Conceptually. action increase sexual arousal. unrelated to levels consistent Sexual Arousal with panic or apprehension. where they have been recognized for years to be based motivation stimuli and sexual-based motor associated with increases in sexual arousal. the Asia strongly linked to sexual inhibition. The current state of knowledge is that the other hand. Other brain neu- rochemicals that are inhibitors of sexual arousal include endocannabinoids and opiates. Another brain neurochemical that facilitates sexual arousal is noradrenaline. factors that inhibit the Centrally acting sex steroid hormones also synthesis. The current state of knowledge is ­sexual arousal. act at the molecular level to . neurochemical facilitator consists of those phar- in part. prevents presynap- may be considered to have regulation from the tic endogenous noradrenaline inhibitory feed- excitatory and inhibitory systems involving critical back. or receptor binding of brain participate in sexual arousal. maceuticals that are dopamine agonists. Antagonists to The female peripheral genital arousal response is these neurochemicals will increase sexual activity observed by genital tissue engorgement and [116–124]. 17 beta estradiol. such as yohimbine. The most prominent and well-studied and progesterone. such as testosterone. stimulate sexual arousal in women with sexual Sexual arousal inhibition involves such neuro. the Latin stimulate serotonin activity decrease sexual America Society for Sexual Medicine. ered centrally acts to stimulate sexual behavior. and the arousal. Agents such as yohimbine facilitate sexual arousal. similar to Physiology serotonin release. other facilitator neurochemicals are mel- to multiple levels of the excitatory dopamine anocortin agonists which have been reported to pathway [116–124]. Centrally acting inhibitor neurochemicals will increase sexual sex steroids. central sexual activation of various dop. dopamine. is associated with increased sexual behavior. opiates. especially orgasm. that in appropriate Central Factors in Female levels centrally. release. factors that acti- tissues including cervix. endocannabinoids. and vate the synthesis. in part. act to decrease sexual arousal and diminish orgasmic capacity. the brain inhibitor neurochemical is serotonin that is European Society for Sexual Medicine. This is a multidimensional process under brain excitatory neurochemicals will increase both central and peripheral regulatory factors sexual excitation. while factors that inhibit serotonin Africa Gulf Society for Sexual Medicine. Such amine pathways in the medial preoptic area and agents are typically used for Parkinson’s disease nucleus accumbens that focus attention to sexual. increased vaginal wall compliance. The most well-known sexual that sexual arousal may be considered to involve. Oxytocin is a well-investigated that is also influenced by numerous complex sexual facilitator neurochemical that when deliv- psychosocial factors. central sexual activation of facilitation and result in lowered sexual arousal. Endo- cannabinoid and opiate activation. noradrenaline. and fluid transudate) from several peripheral genital melanocortins. periurethral glands. dysfunction following intranasal and subcutane- chemicals as serotonin. excitation. agents that are dopamine recep- inhibition of sexual arousal may be considered tor antagonists have been shown to block sexual to involve. On patterns. An alpha 2 receptor Central factors regulating female sexual arousal blocker. Conceptually. and ous administration [116–124]. release. swelling. and thus results in increased noradrenalin central nervous system structures involved in levels.5  Physiology of Female Genital Sexual Arousal 53 Sexual Medicine Society of North America. various inhibitory neurochemicals that feedback Finally.

Clinical studies suggest that estradiol modulates genital hemodynamics. and maintenance of genital muscle that supports the vagina help regulate and nongenital organs and tissues. nora. including genital and estrogens have been shown to produce vasocongestion and vaginal lubrication. keratinization. In addition. In contrast. Centrally Sex steroids both regulate the structure and acting sex steroid hormones bind to specific function of genital organs such as the clitoris. control cellular all effect of the centrally acting sex steroid processes within genital tissues. . Estrogen deprivation leads to decreased pelvic Sex Steroid Hormones and Female blood flow. drotestosterone. Further. are reg. the tone of the nonvascular smooth muscle within Estradiol has specific roles in regulating the the vaginal muscularis and the tone of the skeletal development. thinning of the vaginal wall. androgen. Goldstein and J. During sexual arousal there to modulate development. and skin. arousal. such as growth and function of epithelial cells. central and lature. re-establishing vaginal integ- passing both oncology and sexual health. secretion. clitoris. The over. growth. estrogen progestins (progesterone) for structure and func. physiology of abnormal sex hormones [112–116]. in general. replacement in postmenopausal women increases tion. utilize sex involution and atrophy of the genital organs.(testosterone and adversely affecting cervical. and progesterone. in textbook encom. matrix within the vagina [112–116]. blood vessels. For example. the peripheral ability of the vaginal epithelium. It thus seems reasonable. Sex steroids have been shown to control mucification. and dihydrotestosterone) and estrogens (estradiol)/ glandular mucin production. 112–116. Estrogens are vaginal compliance. to have rity and lubrication [70. Sex steroids have been shown to Peripheral Factors in Female modify vascular and nonvascular smooth muscle Sexual Arousal contractility. and decreased vaginal submucosal vascu- At a fundamental basic science level. and modify the receptor complexes in the cytoplasm that form sexual arousal response including engorgement. smooth muscle cells. sex steroids may regulate the of the erectile tissue and by the tone of blood synthesis and deposition of the connective tissue vessels within the genital tissues. Each cellular hormones is to provide the protein biochemical action affects particular physiological events machinery to enable a state in which sexual stim. dihy- teins and transmitter receptor proteins. and nerves and orgasm [116–124]. endocervical. and function is increased blood flow to the vagina. and perme- In female genital sexual arousal. bone. and progestin hormone external genitalia. Sex steroid the synthesis of different neurotransmitter pro. and melanocortins. and androgens local hemodynamic processes. and vagina. transcriptional agents in the nucleus and lead to swelling. Sex steroids have been shown to regulate synthesis. growth. and reuptake of critical neu- rotransmitters. with menopause is thought to be responsible for many sexual complaints. 125–129]. and vaginal compliance. Silberstein direct the synthesis of multiple proteins such as a chapter review contemporary data relating enzymes and receptors for the various facilitory physiology of sex steroid hormones and patho­ neurochemical systems including oxytocin. such as estradiol. pelvic blood flow. as well as increased vaginal decline in circulating estradiol levels associated compliance. resulting in diminished vaginal lubri- Genital Sexual Arousal cation. [112–116]. of the mammary glands. steroid hormones androgens . testosterone.54 I. The and external genitalia. estrogen deficiency leads to peripheral genital tissues. estrogen. drenaline dopamine. ulation is likely to result in sexual desire. hormones. growth factors and vasoactive and trophic sub- ulated by the tone of the vascular smooth muscle stances. clitoral fibrosis.

an imbalance in nuclei. skeletal muscle. blood. uterus. and mammary gland. must take flow. appears to be associated with sexual behavior [139–142]. Animal studies precursors for the biosynthesis of estrogens. including on sexual arousal. androgens influence bone. Multiple preclinical studies in ovariectomized delta 4 androstenedione. a review is made of physiology control of sexual behavior. Androgens contribute to other androgens (such as delta 5 androstenediol and sexual and nonsexual physiologic functions. that DHEA is involved in the process of vascular In premenopausal women with regular men- smooth muscle relaxation. DHEA receptors cognition. 130–134]. to other androgens. vulvar. thought to also regulate secondary sex characteristics. Androgen receptors have been reported in Dehydroepiandrosterone (DHEA) is an adrenal the vagina and vestibule. adipose tissue. process of vascular smooth muscle relaxation there is a rise in testosterone and androstene- is intimately involved with peripheral sexual dione in the late follicular phase of the menstrual arousal [135–137]. It is possible testosterone precursors such as androstenedione . and main- into account all the actions of DHEA. growth. Androgens hypothalamus and telencephalon. espe. junction with estrogen. areas associated with sexual behavior. enzymes 3 beta and 17 beta hydroxysteroid dehy. energy. Androgens also represent the immediate lation of female sexual behavior. cleic acid-containing neurons are widely distrib- kidney. and testosterone via the animals (rabbits and rats) have been performed.5  Physiology of Female Genital Sexual Arousal 55 Testosterone and dihydrotestosterone have that low values of delta 5 androstenediol are specific roles in regulating the development. such as bone and skeletal muscle metabolism. such as delta 5 androstenediol. Androgens are critical in maintaining peripheral genital tissue structure and function. increases vaginal blood function. The physiologic strual cycles throughout their reproductive years. in con- of sex steroids. cycle and in the luteal phase. numerous regions of the brain integral to central In this chapter. and the remaining 50% is from mucin content of vaginal lubrication. Androgens: Physiology Androstenedione and testosterone levels have and Pathophysiology been shown linked to vaginal physiologic func- tion. Consequently. associated with sexual arousal disorders [138]. of sexual behavior. and feelings of well-being have been found on endothelial cells implying [112–116. and input to the medial preoptic and ventromedial well-being. and vestibular health. These investigations have shown that androgen drogenase. mood. enhances vaginal mucification. In women 50% of Delta 5 androstenediol acts on its own recep. bone density. Testosterone. energy. ovaries. androgen biosynthesis or metabolism in women High densities of the enzyme aromatase are may have undesirable effects on general health observed colocalized with high densities of and on sexual and reproductive functions androgen receptor mRNA-containing neurons in [112–116. Any positive effects of DHEA on sexual smooth muscle relaxation. These regions provide strong adipose tissue distribution. and ultimately to estradiol via treatment enhances vaginal tissue nitric oxide aromatase or to dihydrotestosterone via 5 alpha synthase expression and activity. 130–134]. play a key role mediating the hormonal control Androgens affect sexual desire. cially testosterone and estradiol. facilitates vaginal reductase. uted in the central brain regions such as the vagina. that is tains the health and integrity of the vaginal DHEA alone and as a precursor of multiple muscularis layer. delta 4 androstenedione and estrogens). clitoris. these may play a critical precursor sex steroid hormone that is converted role in vaginal. and maintenance of genital and nongenital Testosterone has been linked to central regu- organs. testosterone synthesis occurs in the ovaries and tors on the vaginal mucosa and is involved in the the adrenal glands. In reveal that androgen receptor message ribonu- women.

The significant decrease in the concentrations of delta symptom improvements in sexual function were 5 androgenic steroids. and body image fol- tosterone was also found in another study. changes in tionships between serum testosterone levels and mood and depression [112–116. sex hormone-binding globulin tion in the constellation of androgen insufficiency increases in postmenopausal women. orgasm. sexual receptivity. Women assigned women with and without symptoms of sexual to testosterone also reported significant decreased disorders. Another even with adequate estrogen treatment. arousal disorder. were noted in total satisfying sexual activity. treatment. Goldstein and J. arousal. A significant correlation between andro. osteoporosis. muscle Several clinical studies have examined the rela- wasting. 130–134]. those who had sexual disorders had a concern or distress about sexual functioning. The frequency of sexual activity onstrated in a study of women in peri-menopause. as well as with free testos. begins to diminish. tosterone. of androgen insufficiency. including decreased one sulfate (DHEA-S) and DHEA also fall with libido. from aging or any Aging adversely affects serum testosterone pathophysiology. In the late repro. and satisfaction. The measure of gland [148–152]. of characteristic clinical symptoms in the pres- ductive years the midcycle rise in free testoster. Clinical symptoms of low free testosterone Androgens: Clinical Data include impaired sexual functioning such as decreased interest. poor lubrication. dys- as a prehormone for about half of ovarian testos. and pleasure. serum dehydroepiandroster. bioavailable testosterone. due to reduced syn. contrast to estrogen and progesterone levels that Androgen insufficiency was defined as a pattern fall abruptly with menopause. In postmenopausal women. predominant in the adrenal considered clinically relevant. terone production. Finally lowing testosterone transdermal patch versus pla- in a small group of healthy premenopausal cebo in postmenopausal women. Silberstein and DHEA processed in the peripheral tissues A multinational expert panel assessed the role [112–116. sexual activity. There many symptoms of low testosterone ovulating women. after menopause androgen motor instability was the symptom of decreased insufficiency occurs. and dihydrotestosterone levels from the lower Index. orgasm. female sexual dysfunctions. significant increases and total testosterone. especially symptoms makes this especially of import to those treated with oral estrogen therapy. free testosterone. the normal range.56 I. and dihydrotes. effect of diminished androgen synthesis and increased sex hormone binding globulin is a reduced amount of free unbound testosterone. sexual desire. Furthermore. persistent unexplained fatigue. in women with sexual health levels in a slow and progressive decline. phoric mood. The net women with sexual arousal disorders [153]. and sexual arousal was dem. vaginal lubrication. ence of decreased bioavailable or free testoster- one. and pleasure was significantly greater than placebo A significant correlation between sexual desire in one study and in another. loss of energy. The inclusion of inadequate lubrica- ries. in sharp concerns including sexual arousal disorders. and DHEA-S were transdermal testosterone patches significantly found in one study with a number of sexual increased free testosterone. women. Correlations between total tes. and vaso- increasing age. terone. 130–134. in part. . improvement in sexual arousal is noted [154–156]. including sexual fre­quency of sexual activity. fantasy. transdermal testosterone therapy signifi- A series of investigations have found correla. changes in sexual function. bioavailable testoster- domains using the Female Sexual Function one. even with adequate estrogen thetic function in both the adrenal and the ova. These factor is the level of adrenal precursors that serve include diminished sense of well-being. limit of the normal range to higher values within gens. cantly improved many sexual functions and tions with diminished levels of androgens and behaviors including sexual motivation. 136. pleasure. a hallmark of the menstrual cycle in young one. pleasure. Thus. In two studies in premenopausal 144–146].

nervosa. estro- cholesterol. . primarily synthesized in terone administration include acne and hirsut. a prospective longitudinal study of serum estradiol. DHEA-S. and polycythemia were ovulate. maintained until the time of menopause. voice premenopausal woman continues to regularly deepening. reported that the testosterone con. but the amount of estradiol synthesized testosterone. 125–129]. high-density lipoprotein cholesterol. postmenopausal women through conversion of Concerning the relation of androgens to androstenedione to estrone and testosterone to aging.” Androgen concentrations may fall and women with such conditions may were highest in the women age 20–29 years. It has been well documented that estro- examined androgen values in women “without gen and progesterone levels in such conditions sexual dysfunction. including female genital sexual arousal dis- demonstrated a marked decline in serum concen. For example. follicular phase of the menstrual cycle and in the fits and the need for routine follow-up and blood luteal phase. tissue structure and function. bone. ical issues during the premenopausal years that Zumoff et al. including total ovarian androgen precursors. No progesterone levels fall abruptly. in part. as well as a study of androgen levels in Premenopausal women with sexual dysfunc- women of all ages using mass spectrometry.4–0.) in ides [148–156]. estradiol and risk of endometrial cancer or endometriosis. should have the aging years. In addition. or triglycer. Other med- testosterone values decrease with age in women. muscle. order who do not have regular. 125–129]. aromatase [70. The calcu.6–0. 112–116. DHEA sulfate and total and unbound underlying pathophysiology managed. adipose tissue. cliteromegaly. on the enzymatic activity of globulin levels through the menopause transi. (skin.6  ng/dl for women induce protein synthesis directed to specific between the ages of 30 and 39 and 40 and 49 central nervous system or peripheral genital years [146. estrogen synthesis occurs via adrenal and line on measures of blood lipids. gen continues to be synthesized in the periphery low-density lipoprotein cholesterol. complaints [70. The luteal phase is characterized by test surveillance testing. As long as the ism. estrogen and progesterone levels are not noted in clinical trials. interfere with cyclical estrogen and progesterone centration of women age 20–29 years was twice production include rapid weight loss and anorexia the value of women age 40–49 years. Safety issues for testos. ovary. 149].8 ng/dl for women age genomic process that utilize transcription to 20–29 years and 0.5  Physiology of Female Genital Sexual Arousal 57 Any woman with sexual arousal concerns of the pituitary via follicle stimulating hormone treated with testosterone therapy needs to be and inhibin. Estradiol also acts in a nongenomic fashion with direct interactions with numerous central neurotransmitter systems including catacholaminergic. and sex hormone-binding depends. the high concentrations of estradiol in the hypothalamus and the preoptic In premenopausal women throughout the repro. Outside of the significant adverse effects were noted from base. the primary source of estradiol is regions is involved in sexual behaviors cyclical synthesis by the ovaries under the control [157–159]. Estrogens/Progestins: Physiology cholinergic. exhibit sexual dysfunction with sexual arousal decreased at approximately age 30. There was no evi. the corpus luteum of the ovary. tion. Guay et al. a rise in progesterone. etc. There is a rise in estradiol in the late thoroughly counseled regarding risks and bene. lated free testosterone in women “without sexual Sex steroids act via cytosolic receptors in a dysfunction” was 0. normal menstrual trations of adrenal C19 sex steroid precursors cycles and are otherwise amenorrheic. 112–116. both tion. When dence that exogenous testosterone increases the ovulation ceases at menopause. and gamma-aminobutyric acidergic and Pathophysiology systems. serotoninergic. area suggest that estradiol in these critical brain ductive years. or dys- and conjugated androgen metabolites during the menorrheic or menorrhagic. Other side effects such as balding.

or rugae normally present in the estrogenized tion of androgen production in the ovaries and vagina.58 I. have no sexual health sloughed epithelial cells is hydrolyzed into glu- issues. smooth muscle cells of the vagina. recognized sex steroids vascular. levels of androgens. The atrophy of the lamina propria blood (2) marked increase in the hepatic synthesis of vessels leads to diminished blood flow to the tis- sex hormone binding globulin. Genital tissue structural changes hormonal milieu. In the postmenopausal women. Diminished estrogen production in the estradiol and progesterone as well as multiple transition/menopause renders these genital tis- delivery systems for administration including sues highly susceptible to atrophy [169–172]. glycogen from are otherwise healthy. decreased lubrication. and urethra. are decreased by oral contraceptives colorless in appearance with loss of multiple folds by two separate mechanisms: (1) direct inhibi. in combina. Thus. Silberstein There is less known about the relationship of low circulating levels of free and bioavailable progesterone with sexual function. discourages growth of pathogenic bacteria. premenopausal women who an estrogen rich environment. Goldstein and J. vesti- gen and progesterone treatment. Thinning of the vaginal epithelial . of vaginal yeast infections. and protection from sexual including bioidentical and synthetic forms of pain. vulva. muscular and connective vaginal tissues. there are many bule. Of note. lubrication. Estrogen provides vaginal choices of estrogen and progesterone for women health. The important principle is that estrogens are required for genital. electing to use exogenous potent synthetic epithelial thinning reduces the available glyco- estrogen. oral. These shift in the vaginal flora resulting in the likelihood oral contraceptives diminish FSH and LH lev. discharge. odor. estradiol increases the expres- sion of progesterone receptor that in turn func- Arousal Disorder Syndrome tions as a critical coordinator of the sexual Associated with Low Estradiol response [160–164]. In addition atrophy of the various including suppression of ovulation. estrogen adversely influence sexual function – this is deficiency leads to vaginal atrophy and an altera- especially pertinent for synthetic progestin tion of the normally acidic vaginal pH that usually agents [165]. or parenteral. and tion of these two mechanisms may lead to very sexual pain. sue to decreased estradiol atrophic changes can gen and progesterone utilized may have impor. vaginal dryness. The change to an alkaline pH value leads to a tion with various synthetic progestogens. many of which can lead to sexual tant implications on the woman’s sex steroid arousal issues. be identified. especially vaginal tissue structure and function. Circulating vaginal tissues occurs including the epithelium. that are major modulators of sexual function in This leads to the vaginal vault becoming pale or women. In As an example. gen. Specifically in the vagina. such as ethinyl estradiol. has genomic activity via progesterone receptors that modulates gene expression and thus regu- lates neuronal networks that control sexual Clinical Female Genital Sexual behavior. Following exposure of peripheral genital tis- The choice of synthetic or nonsynthetic estro. the tal tissues as a result of estrogen deficiency are choice of estrogen and/or progesterone may as follows. and els and reduce metabolic activity of the ovary sexual pain. mal vaginal flora. transvaginal. Estrogens act on estrogen Estrogens/Progestins: Clinical Data receptors that exist in high levels in the genital tissues including epithelial/endothelial cells and Should there be the need for exogenous estro. labia. Progesterone testosterone [166–168]. sues. especially the sex hormone and cellular dysfunctions that occur in the geni- binding globulin and androgen values. trol. The combina. transdermal. and have normal menstrual cycles may cose and then metabolized to lactic acid by nor- opt for a reversible pharmacologic birth con.

Immunohistochemical studies in vaginal and Estrogen deficiency also adversely affects the clitoral tissues have demonstrated the presence bladder and urethral meatus. The endocervical tissue smooth muscle tone and how these neuro- glandular tissue produces less mucin further logic mechanisms are altered by disease states. urinary frequency. It is not uncom. Local estrogen therapy can effectively restore Exogenous norepinephrine causes dose-depen- vaginal epithelium and relieve atrophy within dent contraction in organ bath tissue strips of weeks to months. she experiences pain and/or nal wall tone are largely the result of urgency to urinate and/or inability to have orgasm norepinephrine release from sympathetic nerves secondary to distracting pain. rotransmitters. associated with vasocongestion and changes in Estrogen deficiency also adversely affects the hemodynamics of clitoris and vagina and is other genital tissues. Female genital sexual arousal is a complex event unsatisfactory. neurophysiology of central regulation of genital The labia majora atrophy as there is decreased arousal. note dysuria. The clitoral hood may controlled by a host of parasympathetic and sym- become phimotic and the glans clitoris may atrophy pathetic neurotransmission. Data exist that suggest that is often accompanied by a unique sexual history. inconti. antagonists. surgi. When coital activity is Genital Sexual Arousal attempted in the presence of estrogen deficiency. If necessary. In particular. 185]. edematous After sexual stimulation has ended. neuropeptide Y. It is com. muscle contraction in peripheral genital organs. restoration of vaginal cytology and improvement Contraction to norepinephrine has been shown of vaginal atrophy and dryness. urgency. female genital tissues has been demonstrated. during self-stimulation of the clitoris. vasoactive mon for women with urethral prolapse to note intestinal polypeptide and nitric oxide signaling spotting of blood on the toilet paper after wiping systems to play important roles in regulating following voiding. and sex. Adrenergic Neurotransmitters:  In the nonstimu- during sexual activity with the partner or with a lated state. nitric oxide synthase. There are limited data concerning mon for women to experience itching and pain the regulatory mechanisms modulating genital as tissues undergo atrophy. Several studies have shown clitoral corpus cavernosum and vagina. calcitonin mucosa out the urethral lumen is highly associated gene-related peptide. that cause vascular and nonvascular smooth tion of a urethral prolapse reveals a beefy red. lated strips of rat vaginal tissue [186]. Several studies have and become fibrosed with persistent estrogen provided detailed discussion of the physiology and deficiency and diminished genital blood flow. low genital blood flow and high vagi- mechanical device. postcoital urinary tract infections. prazosin and phentolamine in iso- tibular and/or intravaginal estrogen [179–183]. different female genital organs share these adren- Women with urethral prolapse often have the abil. ­erythematous. termination mucosa. contributing to vaginal dryness.5  Physiology of Female Genital Sexual Arousal 59 layer leads to lowered elasticity and increased Neurotransmitters and Female bleeding of vaginal tissues. The conservative to be attenuated by the alpha-adrenergic receptor treatment involves the use of local topical ves. vasoactive intestinal polypeptide and nitric ity to have full sexual pleasure and satisfaction oxide signaling pathways [184. Currently. and substance P. prolapse of the urethral methionine. ergic. alpha 1 and alpha 2 adrenergic receptors in cal excision may be required [176–178]. choline acetyltransferase. . however. This chapter will focus on peripheral neu- subcutaneous fat and skin elasticity. Women frequently of nerve fibers containing tyrosine hydroxylase. Expression of topical or systemic estrogens. and painful [173–175]. The abnormal voiding history genital blood flow. with estrogen deficiency states. Physical examina. protruding. the most data exist for adrenergic. inflamed. peptide histidine ual pain. active intestinal polypeptide. Conservative treatment options include adrenergic system stimulation. vaso- nence. the marked shortening and narrowing of the vagi- nal vault may make sexual activity unpleasant. prolapsing from the meatus in different of the genital engorged state is also the result of degrees.

Stimulation of the hypogastric nerve the intima with a balloon catheter. mechanism involves activation of G-protein cou- nal blood flow. in vaginal blood flow showed diminished tration-dependent increase in vaginal blood flow. Exogenous vasoactive intestinal female sexual arousal disorder. Animals were results in attenuation of blood flow to the genital. increasing cyclic erosclerotic lesions had significantly diminished guanosine monophosphate resulting in relaxation vaginal and clitoral blood flow following pelvic of vascular and nonvascular smooth muscle. cascade of signaling that produces smooth muscle Atherosclerosis of the ilio-hypogastric-pudendal contraction. A developing hypothesis is that following vagina. especially in the clitoris and the arterial bed was developed following injury to vagina. dysfunction). nonadrenergic.60 I. arousal and a new appreciation for the role of Peptide histidine methionine is a vasoactive organic pathophysiologic conditions resulting in intestinal polypeptide precursor and is colocal. contributing to increased blood flow. norepinephrine binds to alpha 1 lopathic women with both atherosclerosis and and alpha 2 adrenergic receptors and results in a claudication. nerve stimulation. however. In if there is a role for nitric oxide mediation of some women. [194. In the vagina. noncho. normal yet these women may suffer from female Neuropeptides:  Vasoactive intestinal polypep. 195]. the association between cular smooth muscle by acting through the same vascular insufficiency and female genital arousal receptors as vasoactive intestinal polypeptide. nitric oxide activates guanylyl cyclase compared to control animals. Silberstein Nitric Oxide:  Following sexual stimulation.. as well as reduced development . diminished arterial inflow nerve fibers near blood vessels.g. In experiments in isolated clitoral pled receptors which activates adenylyl cyclase cavernosal tissue strips. Genital Vascular Blood Flow engorgement and vaginal blood flow were both increased by administration of a phosphodi- Female sexual arousal is a complex neurovascular esterase type 5 inhibitor. Immunoreactivity for PDE type 5 was local- ized in the endothelium and smooth muscle of blood vessels in human vaginal tissue. In vitro organ bath studies have showed that There is an increased awareness for the role of vasoactive intestinal polypeptide facilitates vagi. however. Similarly. Goldstein and J. vasoactive intestinal polypeptide has been nitric oxide–cGMP signaling appears to be a shown to increase blood flow and the proposed critical mechanism regulating clitoral and vagi. disorders in women has received limited atten- Neuropeptide Y has been detected in human tion. and increases cAMP. Slow oscillations in vaginal tide is likely involved in the regulation of clitoral blood flow have been shown to correlate with and vaginal vascular and nonvascular smooth subjective physiological arousal. slow oscillations polypeptide has been shown to cause a concen. thus modulating vascular linergic relaxation to electrical stimulation was and nonvascular smooth muscle contractility and potentiated by a phosphodiesterase type 5 inhibi. physiologic factors mediating female sexual nal and clitoral smooth muscle relaxation. This is seen clinically in many vascu- In summary. may contribute to impaired genital arousal as tulated that neuropeptide Y regulates blood flow manifested by inadequate genital engorgement in the vagina [190–193]. Vascular insuf- ized in nerve fibers with vasoactive intestinal ficiency states have been associated with disor- polypeptide. vasocongestion) with arousal may appear the vagina [187–189]. it has been pos. maintained on a high cholesterol diet. process that depends on a multitude of factors. animals with ath- in clitoral and vaginal tissues. In women with muscle tone. tor. sexual arousal disorder. female sexual arousal disorders. responsiveness. Due to its primary localization within sexual stimulation. It is not clear. peptide histidine ders and diseases of the penis (erectile methionine can cause relaxation of the nonvas. changes in genital responsiveness relaxation of the nonvascular smooth muscle in (e. When In contrast.

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Central nervous system (CNS) struc- and organ level. most importantly the neurological and vascular systems. and psychological illnesses are linked to ED. 69 DOI 10. Mulhall et al. San Francisco.F. logical and molecular pathways that mediate this critically important process have been elucidated.Chapter 6 Physiology of Erection Alan W. The mechanisms and can have a tremendous impact on erectile func- means by which the penis becomes erect have tionality. superstition. Cancer and Sexual Health. 1.P. thus facili. specifically the medial preoptic area (MPOA) penile anatomy are referred to Chap. USA penile erection as well as ejaculatory function. (eds. In this chapter we will briefly Penile erection may be mediated by both periph- review the current state of the art with respect to eral and central mechanisms. The complex interrelationships of the various Cerebral Control of Penile Erection component tissues of the penis permit the process of penile erection. Given the numerous organ systems been a source of fascination. it is not interest for humans throughout recorded history. Lue Keywords  Corpus cavernosum • Smooth muscle and detumescence are referred to the excellent • Endothelium • Nitric oxide • Adrenaline recent review article by Prieto [1]. thoughts. Further phallus becomes engorged and rigid. University of California Potentiation of dopaminergic function enhances at San Francisco. CA. Shindel and Tom F. Penile erection requires a complex interplay of various organ systems. likely through stimulation of oxytocin. T. more. © Springer Science+Business Media. the medical community Neurological Regulation has been able to potentiate and improve sexual of Erectile Function function in ways scarcely imagined in the past. tissue. The endocrine Introduction system and skeletal muscle play important adjunctive roles in the process of penile erection Penile erection is the process by which the flaccid and in maintaining penile functionality. J. Dopamine appears to play a critical role in the erection- inducing capacity of both the MPOA and the PVN. Readers and the paraventricular nucleus (PVN) of the who desire a more comprehensive understanding hypothalamus. surprising that a substantial number of somatic It is only within the past 40 years that the physio. With improvements in our understanding of the physiology of erection.1007/978-1-60761-916-1_6. Readers desiring a review of tures. and involved in mediating penile erection. LLC 2011 . also play an important role in the of the molecular physiology of penile tumescence regulation of penile erection [2].). psychological state and interpersonal factors tating sexual intercourse. Centrally mediated understanding of the physiology of penile tumes- erections occur secondary to erotic stimuli or cence and detumescence at the molecular. Current Clinical Urology. Lue (*) Department of Urology.

lesions above T9. These centrally hypoxic (pO2 30–40  mmHg) [12].70 A. In this state the penis is moderately what is observed in healthy men. Lue although side effects of currently available cord injury in response to sexually arousing stimuli. with sacral spinal cord injury after electro-stimula- nephrine has also been demonstrated to play a role tion of the MPOA or by administration of apomor- in penile tumescence. although centrally mediated suppression of the sympathetic nervous Tissue Level Mechanisms system also plays a role. as evidenced by the erecto. right insula. stimulation of the penis in these men [11]. Based on these results it has been postulated that visually evoked sexual arousal has three compo- nents associated with neuroanatomic regions: (1) Somatic Nervous System a perceptual-cognitive component that recog. Shindel and T. cord lesions above T9 [10]. was seen in the bilateral inferior temporal corti. suggesting that central inhibition In a study of visually evoked penile erection of sympathetic tone to the penis is the mecha- in response to erotic video clips. 4]. Penile erection is mediated principally by the para- sympathetic nervous system. erections have been detected in ­animals management of ED [3. (2) an emotional/motivational component that pro. CNS release of norepi. With sexual mediated erections may occur in men after spinal arousal. It has been demonstrated that men with sacral spinal cord lesions sometimes The penis is normally in a flaccid state. right inferior frontal cortex. these brain centers are thought be secondary to preservation of the sacral reflex arc to modulate the process of erection by effects on which mediates erectogenic response to tactile centers in the thoracic and sacral spinal cord. these cerebrally induced genic effect of the alpha-2 receptor antagonist erections do not occur in men with spinal cord yohimbine [5]. also responsible for contraction of the bulbospon- giosus and ischiocavernous muscles during maxi- mal arousal. tance in the induction of a reflexogenic erection it may be speculated that other centers integrate mediated by genital touch rather than nontactile stimuli and transmit erectogenic impulses via erotic stimuli [11]. the frontal cortex. leading to engorgement of the corpus spongiosum and the glans penis during the rigid Autonomic Control of Penile erection phase as well as ejaculation at peak arousal. Interestingly. This circuit is of critical impor- tions involving nonvisual sexually arousing cues. Through descend. although by tonic contraction of the corporal tissues and cav- such erections are typically of lesser rigidity than ernous arteries. In situa.F. dopamine agonists have limited their utility in the similarly. phine [8]. brain activation nism underlying psychogenic tumescence [9]. Although the parasympathetic nervous system is of cesses sensory information with motivational primary importance in producing penile erection. This effect is thought to ing projections.W. The somatic nervous system is similar common pathways downstream. and left cingulate cortex). there is dilation of the cavernosal arteries . and stimulation) may be produced in men with spinal left anterior cingulate cortex. mediated maintain the capacity for penile erection. states (occurring in the right insula. and Penile Erection nizes visual stimuli as sexual (occurring in the bilateral inferior temporal cortices). and somatic dorsal nerves of the penis form the first (3) a physiologic component that coordinates portion of the sacral nerve circuit that synapses endocrine and autonomic functions (occurring in with parasympathetic sacral neurons responsible the left anterior cingulate cortex) [6]. Reflexogenic erections (mediated by direct penile ces. for tumescence. The primary parasympa- thetic innervation of the penis is from the sacral of Penile Erection nerve roots S2–4 [7]. right inferior the somatic nervous system also plays a role. Erection Contraction of these muscles is coordinated in Onuf’s nucleus in the S2–4 spinal segments [11].

Neuronal NO is produced ­sinusoids of the paired corpora cavernosa with by activity of the enzyme neuronal nitric oxide fresh arterial blood (pO2 70–100 mmHg). NO release continues to important mediator of penile function. which in turn cleaves GTP to blood the sinusoids expand to the point at which cyclic GMP [16]. kinase.1 characterizes the basic NO-cGMP Molecular Mechanisms related mechanisms underlying penile erection. 14]. With hyperpolarization spongiosum and glans does not occur during the and a decline in intracytoplasmic calcium con- full erection phase due to the relatively thin nature centration. leading to a near com. entrance of extracellular calcium. stimulation of myosin light chain phos- cumflex veins of the penis by the corporal bodies photase (MLCP). cross-bridges occurs. penile erection via continued release from tin and/or smooth muscle content is associated with endothelial cells by the action of endothelial erectile dysfunction in human men [13. Glanular With decline in activity of this MLCK. membrane bound calcium channel which prohibit sary veins quickly follows. While nitric oxide synthase (eNOS). endothelium [22]. including closure of tunica albuginea). collagen and fibrotic processes shear stress from increased blood flow past the are associated with erectile dysfunction [15]. It is readily apparent that abundant smooth mus. inhibition of Rho- by compression of the deep dorsal vein and cir. of the calcium/calmodulin complex. Elastin has signal transduction cascade in the initiation of also received recent attention as a potentially penile erection [20. With increasing influx of guanylate cyclase. Cyclic GMP has a number of they compress the sub-tunical plexus (located down-stream effects mediated primarily by between the spongy erectile tissue and the fibrous protein kinase G (PKG). of Penile Erection Although NO is the best known and studied molecular mediator of penile erection. causing synthase (nNOS) by reaction of oxygen and an enhancement in penile girth and a modest l-argininine. Compression of the tunical emis. eNOS is activated smooth muscle and elastin are generally conducive through an Akt-dependent mechanism due to to erectile function. It is thought that endothelium- derived NO is the principle source for NO neces- sary to maintain penile erection [1]. and phosphorylation of heat and Buck’s fascia. myosin and spongiosal engorgement increases during the light chain tends to be dephosphorylated by the maximal (or rigid) erectile phase. Full engorgement of the corpus shock proteins [17. mic reticulum. . Stimulation of guanylate cyclase by neu- cle content is required to modulate the contracted ronally derived NO is believed to be the initial or relaxed states of the corporal tissues. a number Release of the neurotransmitter nitric oxide (NO) of non-NO mediated signal transduction path- from the nitrergic cavernous nerve terminals is ways have been identified as potential contribu- the initiating step in the molecular pathway leading tors to this process. NO activates the soluble protein increase in penile rigidity. Figure 6. cGMP and PKG have also been tion phase there is typically a slight engorgement of demonstrated to play a role in inhibition of inositol the corpus spongiosum and glans penis mediated triphosphate (IP3) generation. Uncoupling of the actin and myosin with blood via contractile action of the bulbospon. leading to muscular relax- giosus and ischiocavernous muscles [11]. and seques- erection phase) in which intracavernous pressure tration of intracellular calcium in the endoplas- routinely exceeds 100 mmHg. venous drainage channels surrounding it. which inter- this does not permit tight compression of the acts with myosin light chain kinase (MLCK). ation and vasodilation [19]. 18]. During the full erec. during which the action of myosin light chain phosphatase glans penis and corpus spongiosum are engorged (MLCP). opening of plete abolition of venous blood flow out of the membrane-bound potassium channels which corporal bodies and a fully erect penile shaft (full leads to cellular hyperpolarization. It has been play an important role in the maintenance of demonstrated in several studies that decline in elas.6  Physiology of Erection 71 and progressive engorgement of the erectile to penile erection [1]. there is a decline in the concentration of the tunical investment of the corpus spongiosum. 21].

Carbon monoxide (CO) is a breakdown prod. These compounds have all been sanoids that have numerous biological effects demonstrated to induce vasodilation but their mediated in part by a large variety of receptor precise role in normal erectile physiology is sub-types. . CO shares many prop. tion of PGE1 is highly effective in inducing uct of hemoglobin by the action of the enzyme penile erection in humans [29]. Prostaglandins (PG) are a family of eico. tion). Cholinergic neurons have been identified in been demonstrated to induce vascular relax- cavernous nerves and appear to play a sup. dated that acetylcholine acts both by inhibition these molecules lead to activation of adeny- of detumescing adrenergic nerve terminals late cyclase and production of cAMP. 4. including the capacity to endothelium that are thought to play a role ­activate guanylate cyclase.1  Physiology of erection – tumescence mechanisms 1. In the penis. erties dependent on receptor type activa- 3. and has downstream effects similar to cGTP.72 A. Lue Fig. It has been eluci. well known that intracavernous administra- 2. ation after binding to their specific receptors. 11]. this endothelium-derived NO contributes to While the role of PG in mediation of physio- activation of guanylate cyclase in smooth logical erection is at this time unclear. Additional compounds elaborated by the erties with NO. leading to an increase in endothe. cAMP and by direct activation of endothelial cell activates one of several cAMP specific kinases receptors. which to stimulate smooth muscle contraction via produces NO from the substrate l-arginine. EP2 and/or EP4 [27]. and inhibition of HO tinal peptide (VIP).W. it is muscle cells [11]. lial cell production of inositol triphosphate Interestingly. 6. 26]. After receptor binding. PGE1 and PGE2 have unclear [1. Induction of HO in maintenance of penile erection include activity has been demonstrated to enhance endothelium-derived hyperpolarizing factor erectogenic response to the phosphodiesterase (EDHF). and endothelin (which activity has been shown to attenuate the action may have both constrictive or relaxant prop- of all three PDE5 inhibitors in vivo [25. vasoactive intes- type 5 (PDE5) inhibitors. other PG sub-types are known (IP3) [24]. IP3 activates the eNOS. Shindel and T.F. indirect activation of phospholipase C [28]. porting role in erection [23]. prostacyclin (PGI2). heme oxygenase (HO).

Alpha-1 venous plexus. As the compressive force dec­ receptors stimulate activation of a G protein cou- reases venous outflow increases. men with ED [33]. endothelium- of the cavernous tissue. This ated by different mechanisms. late cyclase. This process pled pathway leading to an increase in cellular permits a slow. principally the leads to muscle contraction. Effects that are independent of calcium con- Central control of penile detumescence centration also account for some degree of vaso- seems to rely largely on serotonin. 35]. Calcium binds to calm- Neuronal Regulation odulin and then forms a complex with MLCK. including enhancing release of calcium from the sarcoplasmic reticulum and opening of extracel- lular calcium channels. inhibiting production of cyclic AMP nals derived from these roots have been shown to from GTP. Cessation of cGMP production and breakdown of existing Tissue Level Mechanisms cGMP by PDE5 is likely the primary mechanism of Penile Detumescence of posterection detumescence [32]. there is decreased com. Nerve termi. the sympathetic glandin F2a. phase of inositol triphosphate (IP3) concentration. the process of detumescence by the efficacy of highly selective inhibitors of occurs over three phases. While removal of the erectogenic stimulus is the With phosphorylation of this residue. sympathetic nervous system via fibers derived alpha-2 receptors inhibit the activity of adeny- from the T10–T12 nerve roots [7]. erectolytic neurotransmitter and acts by binding traction of these arteries. In addition to neuronally mediated innervate the cavernous arteries and trabeculae mechanisms of G protein activation. Penile detumes- cence involves return of the penis to the resting state and is mediated in large part by reversal of the erectogenic stimuli previously discussed. myosin cross-bridge formation is potentiated tonic flaccidity of the penis appears to be medi. with cessation of sexual arousal.6  Physiology of Erection 73 Penile Detumescence relationship is complex. using cellular ATP as an energy source. The impor- tance of PDE5 in detumescence is underscored At the tissue level. opposing parasympathetic tone. angiotensin II may also activate the discharge that accompanies ejaculation is thought G protein cascade leading to IP3 production and to play a role in reversing penile erection by increased intracellular calcium. There is an initial PDE5 (PDE5I) in improving erectile function in increase in intracavernous pressure as the cav. has myriad effects on calcium metabolism. At the same time. While Molecular Mechanisms of Penile removal of sexual stimulus is an important part of Detumescence this process. In addition to providing derived substances including endothelin. With cessation of the parasympathetic stimulus a slow reversal in penile erection occurs. to alpha-1 receptors on the cell membrane of pression of the emissary veins and sub-tunical cavernous tissue smooth muscle [34. Activation of the 5-HT2C serotonin receptor has been shown to potentiate erection. IP3 detumescence [30]. followed by a rapid. a number of factors play important roles in expediting this return to baseline. although the constriction that is observed in penile smooth . it of Penile Detumescence is this complex that phosphorylates the regula- tory myosin light chain at the serine-19 residue. actin– principle means of reversing penile erection. whereas activation of the 5-HT1A recep- Loss of penile erection occurs after ejaculation or tors inhibits erection [31]. prosta- tonic suppression of erection. ernous arteries and corporal sinusoids contract Norepinephrine appears to be the principal against the engorged corporal spaces. With con.

It is thought that this “cal. furthermore. tends to potentiate with minimal expenditure of cellular energy the various sympathetically mediated erectolytic [37]. While the funda- smooth muscle myosin phosphatase. and relationship stressors may phosphorylates and thus inhibits activity of compromise erectile function. the physiological manifestation muscle myosin. Shindel and T. tend to stay contracted and vasoconstrictive tone The most parsimonious explanation for these is maintained [36].2. Another majority of cases of ED [38]. be higher in men with psychogenic ED com- pared to healthy controls and men with organic ED. Rho-Kinase sion. With a mental issue in cases such as these may be a psy- decline in phosphatase activity against smooth chological one. higher levels of norepineph- rine are observed in men with psychogenic ED Psychological Factors who do not respond to PGE1 injection compared and Penile Detumescence to those with psychogenic ED who do respond [40]. observations is that sympathetic nervous system cium-sensitizing” pathway is responsible for activation. Lue muscle. which accompanies most stress reac- maintaining penile vascular contraction tonically tions including depression. Experimentally. These effects are thought to be mediated extent in virtually every case of difficulty with in large part by the action of RhoA.F. the actin–myosin cross-bridges of psychogenic ED is based on organic factors. Indeed. Furthermore.2  Physiology of erection – detumescence mechanisms . 6. psychogenic disorders are prevalent to some intrinsic central-mediated inhibition of sacral Fig. comorbid depres- protein that activates Rho-Kinase. the sympathetic nervous Psychogenic causes were thought by Masters system has the capacity to inhibit papaverine and Johnson to be the primary cause of the vast induced penile erection in dogs [41].74 A. anxiety. it has been mechanisms underlying penile detumescence is demonstrated that norepinephrine levels tend to presented in Fig. a small G penile erection.W. 6. A simplified algorithm for the molecular pathways of the penis [39]. While no longer relatively logical explanation is that psychologi- considered the primary etiology in most cases of cal states may lead to an exaggeration of the ED.

the role activity of these various stimuli. Neuroanatomy of penile erection: its relevance to iatrogenic impotence. Arch Sex ing penile tissue integrity include observations Behav. [45–48]. It is clear that a psychorelational situation Penile erection is mediated by a complex inter- conducive to sexual activity is essential in the action of excitatory and inhibitory mechanisms. Smith ER. T has been shown 9. Prieto D. component in normal erectile functioning. 1994. Lacert P. in arterial inflow. are unclear. Tang Y et al. Davidson JM. Physiol Behav. Physiological regulation of penile arteries during sexual situations [43]. in older men with low numeric plethysmography. ally evoked sexual arousal in human males. ated with changes in libido. continuous improvement in our ability to care for although the precise mechanisms for this finding men with erectile problems in the future. Clark JT. production of reliable erections in men. 1985. 1980. may play a direct role in maintaining penile tis. 1989. and veins. it may be speculated that low levels of testosterone may contribute to decreased References interest in sex and hence more difficulty focusing on sexual activity and maintenance of erection 1.131 treated with antiandrogens tend to have declines (2):273–80. . Lee SW. Lue TF et  al. J Pharmacol Methods. 1984. Evidence to support a role for T in maintain. it is not sur- erection is of great importance. Jeanty P et al. and reduced erectile capacity comparison with electrostimulation-induced erection in the rat model. Neuroscience. Assessment of erectogenic drugs by with ED and low T levels. ology but it seems clear that T is an important sympathetic activity it is not surprising that erec.28(1):1–21. decreased smooth phine-induced erection: an experimental study by muscle content. In a meta-analysis of 17 penile erection in the male rat. ease. While the libido-inducing effects of T likely 5. psychological. Danjou P et al.21(1):61–9. It maybe hypothesized that any stimulus which tends to increase cavernous tissue tone will produce a Conclusion similar effect. Pergolide therapy in Parkinson’s dis- there was no statistically significant change [44]. Br J penis [48]. clinical trials of T therapy. Durand J. Penile erection to regulate expression of NOS isoforms in the following complete spinal cord injury in man. While T is associ.6  Physiology of Erection 75 erectogenic stimuli [42]. At the molecular level. The neural mechanism of apomor- increased cellular apoptosis. In the setting of enhanced elucidate the role of T in normal erectile physi- sympathetic activation and suppression of para. Neuroanatomical correlates of visu- sue.82(1):241–54. The pace of discovery regarding mechanisms Endocrine Factors and Penile of penile erection continues to quicken.20(1):17–29. T required for the enhancement of sexual motivation by yohimbine. and situational factors can have a profound effect on a man’s capacity for penile erection. 2008. 8. ment in erectile function was noted in young men 3. J Urol. 1999. Paick JS. increased rates of venous leak. Testosterone is not play some part in potentiating penile erection. Although Penile tumescence is determined by the relative the mechanisms are at this time unclear.231(3):148–52. a significant improve. Int J Impot Res. Given the com- of psychological state in the process of penile plex nature of erectile regulation. time. Further studies are required to properly Urol.35(4):517–21. 1998. prising that numerous biological. that castrated animals or those that have been 7. Chapelle PA. tile function is often compromised. J Urol. 6. It is our hope and belief that this will lead to onadism tend to have poorer erectile function. T and all men with low-normal or normal levels 4.152(6 Pt 1):2125–8. As testosterone (T) has a substantial effect on libido. Oxytocinergic and serotonergic innerva- tion of identified lumbosacral nuclei controlling erection are questionable. its’ direct effects on 2. 1984. J Neurol. and it is Erection near certain that our knowledge of penile and erectile physiology will continue to improve over It has been well established that men with hypog.52(3):216–9. Stoleru S et  al.

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P. In the human male. and resolution. Ejaculation consists of the cated to this aspect of the male sexual response. France take part to the process in a coordinated manner. orgasm. Cancer and Sexual Health. and other substances. Mulhall et al. intense rhythmic contractions of pelvi–perineal the orgasm phase actually refers to ejaculation striated muscles. dissection in testicular cancer. © Springer Science+Business Media. Current Clinical Urology. sug- Dopamine • Spinal cord • Spinothalamic tracts ars. France and involves several organs and other anatomical EA4501. (eds. This is followed by mately connected. France Peripheral Anatomical Organization and Department of Physical Medicine and Rehabilitation.1007/978-1-60761-916-1_7. F. phases. The composition nal tract following retro-peritoneal lymph node of the seminal fluid is complex and contains. Raymond Poincaré At the peripheral level. Concluding the ejaculatory and the intense pleasurable feeling that normally response and marking the sexual climax. The orgasmic response is intimately be defined as forceful propulsion of seminal fluid connected to the ejaculatory response but this will out of the body through the urethral meatus (ante- not be addressed here as another chapter is dedi- grade ejaculation).Chapter 7 Physiology of Ejaculation Pierre Clément and François Giuliano Keywords  Ejaculation • Emission • Serotonin • besides spermatozoa. Neuro-Uro-Andrology Unit. lipids. The seminal secre- tions are secreted in a specific sequence into the The human sexual response can be described as a posterior urethra via phasic contractions of the cycle formed by successive distinct. Garches. exci- seminal expulsion. Orsay. arises accompanies it. These are desire. University of Versailles-St structures belonging to the urogenital tract which Quentin en Yvelines.). Orsay. A correct ejaculatory response in orgasm. 77 DOI 10. A correct ejaculation can changes. This mixture provides spermatozoa with a ­nutritive and protective milieu promoting their survival and Introduction movement during their run through the female reproductive tract to the ovule. Giuliano (*) Pelvipharm laboratories. although inti- glands and the relative ducts. although not suffi- charge but also whole-body physiological cient. a complex neuropsychophysiological human male engaged in sexual intercourse with a process that translates in intense cerebral dis- female partner is obligatory. oligo-elements. the ejaculatory response Hospital. which occurs in the form of tation. a variety of enzymes. Emission corresponds to the secretion of the conditions like after radical prostatectomy or after different components of the seminal fluid from lesion of the sympathetic innervation to the semi- accessory sex glands and testes. J. It synchronized succession of physiological events is nevertheless of crucial importance to state that that form two distinct phases: emission and expul- orgasm can occur without ejaculation in certain sion. for reproduction. LLC 2011 .

78 P. Seminal vesicles are Organs Participating in Emission responsible for the secretion of 50–80% of the entire ejaculatory volume. from the prostate gland contain high concentra- intense contractions of the smooth muscle cells in tion of sugars and zinc providing spermatozoa the wall of the ductus deferens are responsible for with higher motility and longevity. spermatozoa undergo final maturation as they acquire motility and fertilizing Prostate Gland capacity [1]. The prostate gland can be seen as a tangle of fibromuscular tissue that encircles and invests the tubulo-alveolar epithelium. The slightly alkaline secretions storing spermatozoa. median. The epididymis urethra) from the bladder neck to the urogenital is continued by the ductus deferens. and two later- lumen until they reach the caudal segment where als) that surround the proximal urethra (prostatic they are stored prior to ejaculation. Epithelial Ductus (or Vas) Deferens cells release prostatic fluid into about twenty ducts that open onto the prostatic urethra via a It extends from its junction with the caudal part of slit-like aperture in the verumontanum. and then by the distal extremity. the female reproductive tract since spermatozoa The head of the epididymis is followed by a medial are propelled with a first fraction of the sperm segment. Prostatic fluid represents 15–30% of the The terminal portion of the ductus deferens is total amount of seminal fluid expelled during dilated and tortuous (ampulla) and is capable of ejaculation. The ejaculatory ducts open onto the urethra where they mix with most of the the prostatic urethra at close proximity of the spermatozoa to form the first fraction of the prostate gland ducti to form the verumontanum. Bulbo-Urethral (or Cowper’s) Glands Seminal Vesicles These glands are paired structures composed of They are a pair of tubular glands lying posterior tubulo-alveolar epithelium invested by a layer of to the bladder which epithelium is made of goblet striated muscle. the fluid is injected into the ejaculatory duct via strong contractions of smooth muscle cells. The fluid is expressed by epithelial cells membranous portion of the urethra at the base of the into the single tube that is comprised in each penis. Bulbo-urethral glands are actually activated . However. a rapid peristaltic transport of spermatozoa from the caudal epididymis to the ejaculatory duct. At the time of emission. the main source of energy Epididymis for spermatozoa. emission occurs. Clément and F. At that time. sperm. contractions of the smooth the fusion of the ductus deferens with the seminal muscle cells eject the prostatic secretions into vesicle ductus. The seminal vesicle fluid is rich in fructose. the tail (or cauda). the head (or caput). posterior. it is unlikely that seminal vesicle secretions provide the energy This highly coiled tube joins the back of the testis required by spermatozoa for their long travel in through an enlarged extremity. At the the epididymis to the ejaculatory duct formed by time of emission. Giuliano Depending on the phase of ejaculation they seminal vesicle. The emitted fluid can be stored participate in two types of anatomical structures within the lumen of the seminal vesicle until can be distinguished. Bulbo-urethral glands are embed- cells and stroma is composed of smooth muscle ded in the urogenital diaphragm and open into the layers. Contractions of the smooth muscle layer of the epididymis are responsible for the pro- It is more often considered as divided into five gression of spermatozoa throughout the epididymal lobes (anterior. diaphragm. that contains mainly prostatic secretions. the body (or corpus) of the epididymis. In the epididymis.

which cell bodies are located in dorsal ischiocavernosus. prostate gland. is essential for ments of the spinal cord [2. facilitates semen flow to the meatus. 7. the thoracolumbar segments (12th thoracic and . and testes. named Krause-Finger corpuscles [4].7  Physiology of Ejaculation 79 during sexual arousal and their secretions have a Neural Pathways cleaning and lubricating role in the urethra to facilitate sperm flow to the meatus. the bulbospongiosus muscle. Sensory terminals antegrade ejaculation. Intense Efferents contractions of this muscle also contribute to the orgasmic feeling. At the time of expulsion. The dorsal nerve of the penis carries impulses from sensory receptors harboured in The bladder neck. a sensory branch of the somatic pudendal Bladder Neck and Urethra nerve. tus deferens. The tiated by sensory messages coming from various smooth muscle cells layer forming the membra. expulsion phase of ejaculation. More particularly. and levator ani. are found in the medial dorsal horn and ernosus). which encircles the base of the penis (bulb). pudendal nerve [5. but evidenced which reaches the spinal cord via the also of smooth muscle fibres throughout the ure. prepuce. Efferent inputs commanding the peripheral All the pelvic viscera listed above receive events of the ejaculatory response are driven by specific autonomic (both sympathetic and para. and somatic sys- sympathetic for most of them) and somatic tems. facilitate the ejaculatory segments that are. nous urethra wall is surrounded by a layer of stri. a ated muscle (the external urethral sphincter or relatively sparse sensory innervation of the duc- rhabdosphincter). Krause-Finger corpuscles excitatory anterior urethra. sympathetic. which corresponds to an area the penile skin. tors. corpuscles. The strong contractions of present in the glans are made of free nerve end- the bladder neck that firmly tighten bladder out. upper sacral and lower lumbar (in rodents) seg- tion between bladder and urethra. and urethra has been relaxation of the external urethral sphincter. neurons are located in the intermediolateral cell ing synchronized functioning of the organs column and in the central autonomic region of involved in ejaculation. In different mammalian species. Of great importance during inputs driven by myelinated fibres can be poten- ejaculation is the membranous urethra. enters the spi- Striated Muscles nal cord via thoracolumbar dorsal roots [7]. capable of responding to low-­ The male urethra can be divided into three main frequency vibrations. including the neurons. way is constituted by fibres travelling along the hypogastric nerve and. Spinal terminals of the bipolar primary sensory The pelvic floor striated muscles. A second afferent path- thra. Those der when pelvic floor striated muscles contract.1) that drive messages allow. prostatic. 3]. membranous. from the bladder neck to reflex upon mechanical stimulation of the penis. ings in majority but also of encapsulated recep- let prevent seminal fluid backflow into the blad. has a preponderant role in the ejection of semen out of the urethra. and In addition. bulbospongiosus (or bulbocav. 9]. peripheral areas such as penile shaft. are activated during the the dorsal grey commissure [8. after passing through the paravertebral sympathetic chain. the urethral meatus. ganglia. perineum. parasympathetic. The soma of the preganglionic sympathetic innervations (Fig. Afferents The main sensory afferents involved in ejacula- Organs Participating in Expulsion tion are represented by the dorsal nerve of the penis. 6]. and glans up to the of thickened smooth muscle fibres at the junc.

Giuliano Cerebral cortex Thalamus Hypothalamus Pontine nuclei Outputs from pontine nuclei Sensory inputs to thalamus and cerebral cortex T12-L1 Σ Σ PΣ S2-S3 Somatic Pelvic Plexus SV BN VD Sensory P afferents BS Ep Fig. Clément and F. 11]. eral cell column of the sacral segments (first to nective tissue lateral to the rectum.80 P. inferior mesenteric ganglia [12]. 7. The pelvic plexus lies lateral to the third paravertebral sympathetic chain. Emanating The cell bodies of the preganglionic parasym- from the inferior mesenteric ganglia is the hypo. relay in the nerve. The pelvic third segments) of the spinal cord in an area plexus (also known as the inferior hypogastric referred to as the sacral parasympathetic nucleus . and somatic preganglionic and motor neurons is under the influence nerves originating in lumbosacral spinal nuclei command of peripheral and supraspinal inputs. BN bladder neck. integrated at the spinal and brain levels. emerging from the spi.1  Neural pathways controlling ejaculation. plexus arise fibres innervating the anatomical teric ganglia via the intermesenteric nerve to the structures involved in ejaculation. the peripheral anatomical structures responsible for ejac. P prostate. BS bulbospongiosus muscle. VD vas deferens 1st lumbar segments) of the spinal cord [10. parasympathetic (PS). plexus) is formed by the merging of the hypo- The sympathetic fibres. From the pelvic or after relaying in the coeliac superior mesen. Sensory afferents originating in genital areas are SV seminal vesicle. Ep epididymis. pathetic neurons are located in the intermediolat- gastric nerve that lies in the extraperitoneal con. The fibres then anterior sacral foramina with its midpoint at the proceed either directly via the splanchnic nerve tips of the seminal vesicles. gastric nerve and the parasympathetic pelvic nal column via the ventral roots. ulation. Activity of spinal Sympathetic (S).

whether several populations of neurons. Normal activity of these muscles. and descending brain modulating path- ways on SGE are still to be identified. Finally. The brain project to the sympathetic and parasympathetic structures belonging to this cerebral network preganglionic neurons innervating the pelvis [16] comprise discrete regions located within the . spi- and somatic nervous systems. galanin. and urethrectomy [15]. takes with spinal cord transection and humans suffer- place in the spinal cord with specific brain struc. 7. areas and motor centres which are tightly inter- tion (SGE) has been recently identified in the connected (Fig. to reveal brain structures specifically spinal lumbar segments 3 and 4 and that contain involved in ejaculation [22. which cell the pudendal nerve terminate close to LSt cells bodies are found at the sacral or lumbosacral spi. All these data support a well as external urethral sphincter [14].7  Physiology of Ejaculation 81 (SPN) [13]. They are also likely involved pudendal canal in the lateral wall of the ischi. fibres of the sensory branch of Efferents of somatic motoneurons. nucleus innervating the bulbospongiosus muscles onic cells located in the pelvic plexus. As a whole. these spinal nuclei is necessary and sufficient for culectomy. and levator ani muscles as mobile spermatozoa [19]. Supraspinal Organization vic viscera involved in ejaculation are distributed in thoracolumbar and lumbosacral spinal cord as As a centrally integrated and highly coordinated described above. tein. including LSt. which is the product of the immediate early SGE is composed of cells that reside around the gene c-fos rapidly transcribed once a neuron is central canal. 7. in laminae X and VII medial of the activated. the expression of ejaculation as demonstrated by Synchronisation of the activity of autonomic the induction of ejaculation after peripheral. In addition. although a direct connection has not been nal level in the Onuf’s nucleus. 23]. [18]. experimental data collected in different species Because these cells were previously identified as strongly suggest the existence of a cerebral net- projecting to the parvocellular subparafascicular work specifically related to ejaculation that is nucleus of the thalamus. Spinal Organization Cell bodies of neurons that send outputs to pel. lumbar spinothalamic (LSt) cells. exit the ventral proved yet. exist in SGE is still Central Nervous System Network unclear. Despite tures having an essential influence.e. or pharmacological stimulation in animals for correct ejaculatory response to occur. An additional spinal centre. as well as to the motoneurons of the dorsomedial travelling in the pelvic nerve. ejaculation involves cerebral sensory also known as the spinal generator for ejacula. is maintained where the pleasurable feeling raises. vesi. 21].2). which is necessary nal. The SPN neurons send projections. further advances are required for clarifying some aspects of SGE func- tioning. Integrity of in patients subject to cystoprostatectomy. ejaculatory response allowing the collection of ischiocavernosus.3). Indeed. Research teams have used male rat that seems to orchestrate the activity of immunohistochemistry directed against Fos pro- autonomic and somatic neurons [16] (Fig. mounts and intromissions in rats. [9]. recent decisive progress. cholecystokinin. they are referred to activated whatever the preceding sexual activity. to the postgangli. process. and enkephalin [17]. in the orgasmic response as a relay for sensory orectal fossa. ing from spinal cord lesion [20. recent investigations in anaes- horn of the medulla and proceed via the motor thetized male rats have demonstrated that electri- branch of the pudendal nerve to the pelvic floor cal stimulation of SGE elicits a complete striated muscles. stimuli from the periphery to the brain structures as measured with EMG electrodes. LSt cells also i. The crucial role for LSt cells that orchestrate secretory pudendal nerve enters the perineum via the and motor outputs. including bulbospongiosus.

IMG intermesenteric ganglion. SPN sacral parasympathetic nucleus Sexual cues Cerebral cortex Thalamus ° SPFp Hypothalamus BNSTpm MeApd ° MPOA ° PVN PNpd Midbrain ° PAG Pons ° nPGi Sensory inputs from Motor outputs to spinal nuclei genital areas commanding ejaculation Fig. SPFp parvicellu- posterodorsal medial amygdaloid nucleus.82 P. Clément and F. Giuliano Fig. 7. preoptic area. tocellular nucleus. MeApd PVN paraventricular thalamic nucleus. nPGi paragigan- tral pathways involved in ejaculation. 7.2  Schematic view of LSt cells situation and connections to spinal centres of ejaculation in the male rat. PP pelvic plexus. PAG periaqueductal grey.3  Diagram of brain structures and putative cen. medial bed nucleus of stria terminalis. BNSTpm postero. PNpd posterodorsal preoptic nucleus. MPOA medial lar part of the subparafascicular thalamus .

However. it was shown that MPOA proj. research has indicated that dopamine (DA) plays In the brainstem. Here. PVN also sends direct projection to ual behaviour. we will describe the transmitters that have These data suggest a pivotal role for SPFp although received a particular attention and whose mecha- functional investigations are lacking. five DA . different nuclei have received an important role in the central regulation of the increasing attention. The other nisms of action are clarified in some aspects. Actually. Neurochemical Regulation vate autonomic preganglionic neurons in the lum- bosacral spinal cord [35. it can both emission and expulsion phases of ejaculation be suggested that a baseline brain inhibitory tone were abolished after MPOA lesion [26] and elic. 30] release is required for ejaculation to occur. PAG constitutes a relay been documented in several experiments where between MPOA and nPGi [25. 42]. an extensive body of of genital sensory signals to the MPOA. out- SGE). and can trigger ejaculation in anaesthetized rats. Thus. on ejaculation has been suggested in several nucleus (PNpd). 43]. and the parvicellular part of the rat experimental models [40. which projects to motoneurons and (BNSTpm). details of the mechanism. side sexual context and in the absence of genital ects to other brain regions involved in ejaculation stimulation [46–48]. 39] and receives inputs from LSt cells [17]. midbrain structures such as the paraventricular hypothalamic nucleus exert a regulating function on ejaculation but fur- (PVN) [31]. Reciprocal data provide further support to this view by show- connections between those substructures and the ing increased expression of Fos protein in nPGi of medial preoptic area (MPOA) of the hypothala. A strong inhibitory role for male sexual response [49. To date. and PNpd [22. An inhibitory ling sexual behaviour [24]. to take part in regulation of the ejaculatory process in rat are MeA. the posterodorsal preoptic 41]. Behavioural subparafascicular thalamus (SPFp). on spinal mechanism of ejaculation exists and its ited after chemical [27. [3. nucleus (MeApd). The PVN has long been known as a key site for neuroendocrine and autonomic integration [34]. the posterodorsal medial amygdaloid interneurons in the lumbosacral spinal cord [40. a brain excitatory influence on spinal studies failed to reveal the existence of direct con. However. 25]. the exact role of these nPGi in the brainstem [37]. as established in neuro- The pivotal role of MPOA in ejaculation has anatomical studies. Bilateral chemical various substances in ejaculation is difficult to lesion of the PVN with NMDA was associated define because of the wide range of sexual param- with one-third reduction in the weight of the sem- eters (other than ejaculatory ones) affected. stimulations of this brain area. 45]. Dopaminergic Control BNST. Their precise roles remain unclear but they may be involved in the relay Over the last decades. Clearly. 28] or electrical [29. based on Fos pattern of expression. forebrain structures which have been proposed. control of ejaculation also likely exists since nections between the MPOA and the spinal ejacu. 50]. intracerebral administration of dopamine agonists latory centres (autonomic and somatic nuclei. has been reported in influence on ejaculatory reflex was demonstrated anatomical and functional studies [23. ther investigations are required for revealing the and the paragigantocellular nucleus (nPGi) [33].7  Physiology of Ejaculation 83 posteromedial bed nucleus of stria terminalis nPGi. sends projections to BNST. the periaqueductal grey (PAG) [32]. male rats copulating but not in animals repeatedly mus. 36] and pudendal A variety of transmitters distributed throughout motoneurons located in the L5–L6 spinal segment supraspinal and spinal sites are essential for sex- in rats [9]. Neuroanatomical However. conflicting results depending on antegrade tracing studies have shown that SPFp the site in the CNS where the transmitter acts. a brain area known as essential in control. Retrograde and cies differences. for PAG [44]. and MPOA and the existence of multiple receptor subtypes. Parvocellular neurons of the PVN directly inner. (>2 times) ejaculating [22. spe- inal material ejaculated [38]. 25]. MeA.

In addition. It is however unreli- induces ejaculation in anaesthetized rats when able to ascribe one particular influence of 5-HT delivered into the cerebral ventricles or into receptor subtypes on ejaculation since a number MPOA and this effect is reversed by D3 but not of data indicate that they either activate or inhibit D2 preferential antagonists [47. Different 5-HT receptor tors in male sexual behaviour. tory response. widely prescribed as antidepressants. A couple of decades ago. plays a role as a neuropeptide in the CNS [66]. the effects of the subtypes may have opposite action on ejacula- preferential D3 receptor agonist 7-OH-DPAT tion. 5-HT rather seems to exert an activating activity of DA agonists [53]. tion in the CNS. triggers D2 and D3 receptors cannot be ruled out. 62]. the tors in male rat sexual motivation is well estab. but not D1-like receptors. compound facilitates ejaculation without affect. increased spi- facilitate ejaculation [55. the use of such a biological role of cerebral serotonin (5-HT) on ejaculation marker makes it impossible to determine the [61. which include the brain to inhibit ejaculation [63]. which causes sudden conscious rats [54] although the participation of release of 5-HT in the synaptic cleft. mediate the pro-erectile level. ture ejaculation and. In an serotonin or SSRI. Induction of erection role on ejaculation. Advantage has been receptors) based on their. 5-HT1A. and D4 ticularly ejaculation in men. 7-OHDPAT control of ejaculation [65]. especially after structurally characterized and classified into two repeated administration. Very recently. However. and D4 clarified but these compounds very likely act in subtypes. ejaculation in anaesthetized rat with complete stimulation of D2-like receptors was shown to spinal cord lesion [64]. 52]. and have long been distinct families (D1-like comprising D1 and D5 known to impair sexual functions and more par- receptors and D2-like comprising D2. The amphetamine derivative by a selective D4 agonist was recently reported in p-chloroamphetamine. In addition. The selective serotonin re-uptake inhibitors causative link between OT system and ejacula- (SSRIs). facilitate expulsion reflex in effort to better characterize the role of D3 recep. The involvement of D2 and/or D3 recep. the ejaculatory response depending on their loca- the use of a highly selective D3 receptor antago. which include D2. Quantification of the level of expression of the immediate early gene product Fos protein Serotonergic Control revealed a link between ejaculation occurrence and the neuronal activity of OT neurons in the A great body of evidence supports the inhibitory PVN [67]. respectively. Amongst the 14 structurally distinct 5-HT were studied. anaesthetized rats [63]. D3.84 P. Blockade of those receptors results in specific inhibition of the expulsion phase of ejaculation Oxytocinergic Control that translates in lengthened ejaculation latency in male rats free to copulate with sexually receptive The nonapeptide oxytocin (OT) is a major hor- females [60]. Giuliano receptors (designated D1–D5) have been induce increase in 5-HT tone. Several pharmacological studies . this receptor subtypes identified to date. When injected systemically. 48]. nist shed light on the role of D3 receptors. 1B. 57]. D3. It appears therefore that a particular mone secreted by the hypothalamic–neurohypo- component of the brain dopaminergic pathway is physeal system. following intrathecal delivery of ejaculation in anaesthetized rats [46. SSRIs to impact ejaculatory function is to be D2-like receptors. SSRI dapoxetine has received marketing authori- lished. In rats. At the spinal D1 and D5 subtypes. and 2C subtypes have been shown involved in the ing sexual arousal [58. Clément and F. positive taken from these observations for the develop- and negative coupling with adenylate cyclase ment of pharmacological management of prema- activity. The D2/D3 antagonist haloperidol reduces zation for this condition in Europe and other parts the interest of a male rat towards an oestrous female of the world. 59]. at the time of writing. 56] and can even trigger nal 5-HT levels. The exact mechanism of action for and sexually conditioned stimulus [51. especially involved in the control of a specific increasing evidence demonstrated that OT also aspect of the ejaculatory response.

However. the VTA contains A10 DAergic controls the autonomic. visceral sensory responses. The lack of MPOA activation dur- sion tomography (PET) in healthy male volun. sexual arousal [78]. Quite unexpected is the ulatory response with forceful expulsion of intense increase in blood flow in an extended semen. understanding of the brain functioning during medial. In an experimental paradigm developed . neuronal substrate for the euphoric state related ejaculation) is complicated because of the inti. These observations make the VTA a key element of the neuronal substrate for orgasm. and con. imaging studies in men. involved in sensory and emotional processing 71] where the neuropeptide may interact with [76] and thus its activation concomitant to ejacu- dopaminergic system [72]. SPFp can also be Sensory inputs have been shown sufficient to suggested as an important relay in the human provoke expulsion reflex or even complete ejac- male orgasmic response. ing ejaculation was also found in Fos study per- teers who received penile stimulation from their formed in monkeys [79] and let us suggest the female partner until ejaculation occurred. 80]. noticed that some results of the brain imaging rectly designed experimental paradigms render study of Holstege and collaborators are in dis- possible the specific study of neuronal activity in agreement with data obtained in rodents using relation with ejaculation. the strongest activation was of the ejaculatory response in primates. motor and coordination control as well as pro­ ing OT receptors but also vasopressin receptors prioception. Fos immunohistochemistry [22. OT acts in accessory sex glands contain.g. and has previously been shown activated in human during cocaine or heroin rush [74. At the lesser importance of this structure in the control time of ejaculation.7  Physiology of Ejaculation 85 using OT receptor ligands clarified the situation zone (vermis and cortex) of the cerebellum dur- and indicated a facilitating role of OT on ejacu. Notably. the cerebellum has also been shown [68. In their PET imaging study. The Trigger for Expulsion based on data collected in rats (as described in supraspinal organization). This study used positron emis. erection. Human found in mesodiencephalic transition zone imaging studies have provided key data for the including ventral tegmental area (VTA). is also deactivated dur- tions have been used for identifying the brain ing cocaine rush [74] and in correlation with areas involved in the human sexual response. lation may be related to the orgasmic response. in blood flow. In addition. cor. SPFp. which to date that aimed at investigating the changes in were found specifically activated in relation with regional cerebral blood flow in human during ejaculation in male rats. arousal. 23]. as demonstrated in previous with relatively high spatial and temporal resolu. somatic. The release of amygdala The discrimination of the different components influence on other brain areas may constitute the of the sexual response (e. do not display changes ejaculation [73]. and sensory cell group belonging to the mesolimbic system responses during ejaculation. to different contexts including orgasm. and ventral thalamus. Most nota- only one brain imaging study has been performed bly. In addition to its primary role in lation. more importantly. tion and sexual arousal [78. ing ejaculation. It is to be mate relationship between them. as indicated by decreased Human Brain Functioning blood flow. 75]. BNST and subregion of the MPOA. Holstege and col- laborators noted that amygdala was deactivated during ejaculation. fur- trol of pelvic floor motoneurons and sympathetic ther investigations in men are required for preganglionic neurons throughout the spinal determining how the spinal neuronal network cord. Those thalamic ejaculation and orgasm but also its participation areas are known to be associated with rewarding to other aspects of the sexual response like erec- processes. 69] and. This element of the limbic system is essential for the processing of emotional reac- Noninvasive functional brain imaging techniques tions [77] and. in the brain [70. However. To our knowledge.

but we rather postulate this expulsatory reflex as gering event as the build up of a prostatic pres. This method. 91].86 P. The within the urethrogenital tract. The purpose here is not to reject the fact data available. contractions of bulbospon- taken in healthy volunteers did not evidence giosus muscles identified with electromyo- the formation of a prostatic pressure chamber graphic electrodes were evidenced following before semen expulsion [92. definitive answer on the identity of the expulsion Despite the number of experimental and clinical trigger. In anaesthetized and intact rat. muscle contractions [85] suggesting that in These procedures are currently used in routine case of dry ejaculation another mechanism to evaluate the integrity of neural pathways takes place to trigger expulsion phase. stipulates the trig. sion phase of ejaculation can occur in the absence 86]. controlling ejaculation and have also served as 5. it has been demon- mic contractions of bulbospongiosus muscles strated that: [21]. consists in placing a vibration-delivering sion in those patients [15]. Distension of urethra with small volume of mechanical distension of the posterior urethra. electrostimulation of the penile dorsal nerve. pudendal 1. the exact neurophysiological that stimulation of the urethra can initiate con- event that can be regarded as the trigger for tractions of pelvic striated muscles – there are expulsion is still not clearly identified. Indeed. obligatory relay in the brain [82]. namely penile vibratory stim- pre-operatively despite the absence of emis- ulation. Penile vibratory stimulation allowed to of urethral stimulation and that the prostatic obtain complete ejaculatory response in more pressure chamber concept does not provide a than 50% of men with spinal cord injury [20]. clear evidence in favour of this phenomenon – proposed by Marberger [87]. com. dorsal nerve of the penis and pelvic nerve which 2. several lines of evidence. causes a series of rhythmic tification in rat of a spinal ejaculatory generator reflex contractions of the pelvic striated muscles in adapted position for integrating peripheral and responsible for forceful propelling of urethral supraspinal inputs and commanding autonomic . The recent iden- ejaculatory centres. respectively [81]. sure chamber created by seminal secretions in the absence of any sexual cue. However. 93]. 3. Anaesthesia of urethra by infusion with lido- nerve (motor branch innervating bulbospongiosus caine did not prevent bulbospongiosus muscle and ischiocavernosus muscles) firing was mea- contractions elicited by urethral distension in sured in response to electrical stimulation of the rat [89]. 4. Giuliano in anaesthetized rat with transection of the spinal content. either the dor- sum or frenulum. Clément and F. More recently. The search for resulting distension of the bulbous urethra. saline is unable to provoke bulbospongiosus and magnetostimulation of the sacral root [83–85]. A theory.5  mm ampli. did not prevent occurrence of pelvic striated it was shown that electrical stimuli delivered to muscle contractions resulting in dry ejacula- the pelvic afferents carried by the intermesenteric tion nor did it alter the related orgasmic sen- nerve can evoke the expulsion reflex after an sation [90. to prevent pos- entering the posterior (bulbous) urethra with sibly deleterious accumulation of seminal fluid concomitant closure of the bladder neck. Altogether these findings indicate that the expul- tude vibrations for 5–15 min in 1–3 series [20. Pharmacological inhibition of seminal emis- convey sensory information from penis and ure- sion by alpha adrenergic receptor antagonists throgenital tract. Endorectal ultrasonography studies under- In humans also. ally contradict it. and applying 2. a secondary mechanism which may take place. actu- ing liquid perfused into the urethra elicited rhyth. another possible site triggering ejaculation has municated through sensory pathways to spinal given rise to interesting studies. recently discussed in greater details [88]. device on the glans of the penis. pattern basis for developing a method that produces and intensity of perineal striated muscle con- ejaculation in patient with neurogenic anejacula- tractions were found similar to that measured tion. urethral distension by accumulat. In patients after cystoprostatectomy. cord at T8 level.

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Part II Disorders of Sexual Function .

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but evolving and an ongoing discus- diseases). Blegdamsvej 9. neurological diseases. A well-defined classification is Psychiatric Centre Copenhagen. development of assessment J. both functional and dysfunctional. Consequently the definitions of FSD are not depression. They radiation. and women with high Numerous epidemiological studies have shown level of sexual interest were considered nympho- that women’s sexual function and dysfunction are maniac as short as a century ago. 93 DOI 10. also necessary for research and measurement of 7411. Giraldi (*) clinical work. (eds. family issues. antidepressants). body image. they are necessary. psychological. rooted in (lack of sexual desire in women) are now consid- biological. ception issues. All may vary within different cultures understanding of women’s sexual function and and over changing time periods. are today influenced by various factors: biological factors ­considered as normal and desirable. iours that were previously considered normal Women’s sexuality is multifaceted. 2100. pelvic difficult to define. include medical and psychiatric diseases (e.Chapter 8 Classifying Female Sexual Dysfunction Annamaria Giraldi MD. ered as dysfunctional. sion of them continues to take place.g.). the subjec- Over the past decade classification of female tive nature of sexual experience. clinician and the patient and between clini- cians. contex- They make the clinician capable of differentia­ tual factors (social) include ethnic and religious ting between transient sexual complaints. and partner’s health and They facilitate communication between the sexual health [1–7]. Sexological Clinic. Cancer and Sexual Health. life stage a distressing and persistent sexual problem. the fact that classifications are evolving and substance abuse. stressors. relationship with partner. surgical procedures). hormonal changes. Sexual behav- behaviour. Despite pharmacological treatment (e. Mulhall et al. © Springer Science+Business Media. and social factors.g.1007/978-1-60761-916-1_8. Current Clinical Urology. menopausal status. as they create the common basis for A. personality.D Keywords  Arousal • Orgasm • Pain • Sexual Pain Classification of sexual dysfunctions is a • Sexual Desire • Classification • Definition d­ ifficult and challenging task. which mirrors the present tion [8]. and coping strategies. urogenital constant.g. economical and household factors. contra- are part of normal life from sexual dysfunction. LLC 2011 . psychological serve the purpose of conceptualizing the cur- factors include sexual development. and the classifica- tion of FSD is no exception. The consensus of what is considered as healthy (normal) or dys- Introduction functional is changing and varies according to different paradigms that are themselves derived from the perceived normal reference. Ph. rent understanding of sexual behaviour and sexual experiences including abuse. which norms. and different sexual dysfunction (FSD) has undergone intense perspectives on sexuality and its conceptualiza- scrutiny and revision. Copenhagen. Denmark treatment outcome.P. and medical therapies (e. function. sexual education.

Historical Overview of the Development of Classification of FSD The DSM System Very early. and impotence a fourth category. to the three phases and functional dyspareunia ders included two sets of diagnostic terms for and functional vaginismus. however. but lack of sexual inter. Subsequently the sexual dysfunctions bance itself. being the physiological genital arousal. which . a linear model introduced for the first time as a further subtype based on physiological observations. 8. the B criterion. [10]. plateau. and orgasm (and resolution) using three criteria: The A criterion. In the revised edition. Human Sexual Response [11] and later acquired. which were added as sexual dysfunction. the sexual dysfunctions were inclu. Fig. psychogenic or psychogenic/biogenic were duced the sexual response cycle. Giraldi instruments. inhibited sexual excitement (fri- ual dysfunction [9]. An entire section was and Lief [14] later drew awareness to sexual devoted to sexual disorders in this edition. the namic psychiatry. excitement. On the basis of this a triphasic sexual sonal difficulties caused by the sexual disorder. classifications are neces- sary for treatment and reimbursement in most health care systems around the world.1). In addition more or sexual performance. DSM-III-R [16]. In the second edition gidity).1  The sexual response cycle. DSM-IV [17] and DSM-IV-TR [18] consider- and orgasm followed by resolution. This also reflected the described as “disturbances in sexual desire and in clinical experience that the primary complaint of the psychophysiology. the perception of the term inhibited was dropped and what was in the sexual problems was that it was psychophysio. In the DSM-III-R the terms lifelong or book. which requires that were then linked to each phase and since then the “the disturbance causes marked distress or inter- phases have been the basis of how we describe personal difficulty” and the C criterion. dyspareunia. and inhibited orgasm which all are linked (DSM-II) the section psychophysiologic disor. The desire. response model was developed describing: Consequently the sexual disorder was described desire. In the first edition and classify sexual dysfunctions. They intro. Both DSM-I and DSM-II reflect psychody. sexual desire.94 A. DSM-III [15] (DSM-I) in 1952 there was a section on sexual included the psychosexual disorders: inhibited deviations but without a description/term of sex. the distur- (Fig. and Human Sexual Inadequacy [12]. changes that characterize women was not a problem with genital response the sexual response cycle” [8]. Kaplan [13] ably changed the picture. The model classification of each dysfunction to make a was divided in successive stages: excitement more precise description of the dysfunction. and generalized or situational. 8. Kaplan [13] Association’s Diagnostic and Statistical Manual of Mental Disorders (DSM). and the psychosexual disorder was by Masters & Johnson. previous editions described as a psychosexual logic in nature [8]. emphasis was put on the distress and interper- est/desire. dysfunction was now termed a “sexual dysfunc- In 1966 Masters and Johnson published their tion”. On the economics level. describing a psychological process concept that psychological inhibition was the embracing sexual thoughts and sexual fantasies primary cause of psychopathologic disorders was preceding the physiological processes described abandoned. Adapted from Masters ded and defined in the American Psychiatric and Johnson [11]. and new treatment modalities.

women’s sexual medical or psychological factors seemed unjusti. non-coital sexual pain. but instead are receptive to sexual stimuli. Furthermore the described sexual behaviour is directed towards the heterosexual couple and intercourse is the reference. resulted in a definition including objective can be difficult to separate desire and arousal and and subjective arousal as described in Table 8. This model was chal- since a substantial overlap very often exists. American Foundation for Urological Disease in The determination as to whether the condition 1998 to review and suggest an update of the clas- warranted a diagnosis was made by the clinician. and many other parameters known Despite the suggested changes. Moreover. it is rec. shown that the correlation between genital sentations of the same phenomena. response is described as a linear progression of fied. followed by caused by biological or psychological causes arousal. there may be interaction between the phases. genital swelling. they added included the diagnosis Sexual Dysfunction due to receptive desire as a crucial part of women’s sex- a General Medical Condition. phases based on the Masters & Johnson/Kaplan ognized that it is very often impossible to separate model. dominated by different physiological the aetiology of the dysfunction into what is responses.2) .8  Classifying Female Sexual Dysfunction 95 indicates that the disturbance is not “better The First Consensus Conference accounted for by other Axis I disorders (except another sexual dysfunction) and is not due exclu- On the basis of the focus on these limitations a sively to the direct physiological effect of a sub- consensus conference was organized by the stance abuse or a general medical condition” [18]. they suggested evidence that medical conditions and substance modifications of the DSM-IV diagnoses as out- use can affect sexual function. The committee included taking into account factors that affect sexual European and North American academic and functioning such as age and the context of the clinical experts from several disciplines. 8. the fact that they continued to rely on the tradi- Taking into account that there was growing tional model of sexual response. It Traditionally arousal has been seen as the bodily has been argued that the DSM diagnoses have signs of arousal (lubrication. DSM-IV-TR also lined in Table 8. Substance-Induced ual response based on research showing that Sexual Dysfunction. With the knowledge we have today. social factor. lenged by Basson [20]. the fact that several studies have male and female dysfunctions as parallel repre. and Sexual Dysfunction not women may experience spontaneous sexual otherwise specified [18]. relationship. failed in several aspects: It is inaccurate to ­present etc.1. and it tent. contextual factors. it has been Circular Model Versus a Linear Model pointed out that important factors. However. neglecting the effect of past and current sexual Conference experiences. They also emphasized the impor- Definitions Reconsidering tance of sufficient sexual stimulation and arousal the DSM Definitions as essential to the diagnosis of orgasmic disorder.1). Finally. that ­sexual responses and subjective arousal is very inconsis- response does not follow the linear model. during recent years based on several critiques.). desire and fantasies. such as emo- and the Second Consensus tional and interpersonal aspects are ignored. dissatisfaction to affect women’s sexuality [8]. although many do not expe- rience this regularly. sification of FSD [19].1. initiated by desire. What is also remained with the revised diagnoses. Despite person’s life [18] (Table 8. they struggled The DSM-IV diagnoses have been challenged with the difficulties of describing sexual arousal. They introduced a third sexual pain category. and then orgasm. In her model (Fig. Most importantly. In the important is that the separation between primarily models described above.

an maintain minimal vulval swelling or vaginal adequate lubrication. The lack factors that affect sexual receptivity to of interest is beyond a normative functioning such as age sexual activity. intrusive. The awareness of subjective arousal is typically but not invariably unpleas- ant. stimulation and reduced sexual sexual excitement causing personal sensations from caressing genitalia. absence of disorder for sexual activity. International Consensus Committee [18]b ence 2000 [19] 2003c. Criterion Aa Consensus confer.g. Self-report may include (FSAD) of the sexual activity. responses Vaginal lubrication or other signs of physical response still occur Combined genital and subjective arousal disorder Absence of or markedly diminished feelings of sexual arousal (sexual excitement and sexual pleasure) from any type of stimulation as well as absence of or impaired genital sexual arousal (vulval swelling and lubrication) Persistent genital arousal disorder Spontaneous. feelings of sexual arousal (sexual tion/swelling) or excitement and sexual pleasure) other somatic from any type of sexual stimulation. distress. The absence) of sexual thoughts or fantasies and a lack (HSDD) judgement of deficiency sexual fantasies/ of responsive desire.1  Definitions of female sexual dysfunction Revised definitions from AFUD/AUAF DSM-IV (TR). lessening with life cycle and and the context of the which causes relationship duration person’s life into account personal distress Sexual aversion Persistent or recurrent Persistent or recurrent Extreme anxiety and/or disgust at the disorder extreme aversion to and phobic aversion to anticipation of/or attempt to have any avoidance of all (or almost and avoidance of sexual activity all) genital contact with a sexual contact sexual partner with a sexual partner. throbbing. and/or attempting to become sexually clinician. or Absence of or markedly diminished genital (lubrica. taking the desire for or aroused are scarce or absent. d [21] Hypoactive Persistent or recurrently The persistent or Sexual desire/interest disorder sexual deficient (or absent) recurrent   Absence of or diminished feelings of desire sexual fantasies and desire deficiency (or sexual interest or desire. The arousal is unrelieved by one or more orgasms and the feelings of arousal persist for hours or days (continued) . which causes sexual distress Female sexual Persistent or recurrent The persistent or Genital sexual arousal disorder arousal inability to attain. pulsating) in the absence of sexual interest and desire. and unwanted genital arousal (e. sufficient sexual lubrication from any type of sexual swelling response of excitement. Motivations for or absence is made by the thoughts. Giraldi Table 8.96 A. tingling. which Subjective sexual excitement still may be expressed occurs from nongenital sexual as a lack of stimuli subjective Subjective sexual arousal disorder excitement. or to recurrent inability Absence of or impaired genital sexual disorder maintain until completion to attain or arousal.

and unsatisfactory sexual and emotional contexts 3. which the clinicians judgement causes personal that the woman’s distress orgasmic capacity is less than would be reasonable for her age. and cultural/religious restrictions 2. medications. ruled out/addressed which causes personal distress Noncoital pain NA Recurrent or NA disorder persistent genital pain induced by noncoital sexual stimulation NA non-applicable a  The definition also has to include: Criterion B: The disturbance causes marked distress or interpersonal difficulty and criterion C: The disturbance is not better accounted for by another axis I disorder (except another sexual dysfunction) and is not due exclusively to the direct physiological effects of a substance abuse or a general medical condition b Subtypes: lifelong/acquired. or absence of. and/or any musculature of the outer involuntary spasm object. and the adequacy of sexual stimulation she receives Sexual pain disorders Dyspareunia Recurrent or persistent genital Recurrent or Persistent or recurrent pain with pain associated with persistent genital attempted or complete vaginal entry sexual intercourse. despite the woman’s expressed third of the vagina that of the muscula. generalized/situational c Subjective distress should be measured and rated as: none. wish to do so. a finger. orgasm recurrent arousal/excitement. Medical conditions. The pain associated and/or penile-vaginal intercourse disturbance is not caused with sexual exclusively by vaginismus intercourse or lack of lubrication Vaginismus Recurrent or persistent Recurrent or Persistent difficulties to allow vaginal involuntary spasm of the persistent entry of a penis. Negative upbringing/losses/trauma. delay of orgasm. sexual experience.8  Classifying Female Sexual Dysfunction 97 Table 8. partner’s sexual dysfunction. inadequate stimulation. Women in. psychiatric conditions. The diagnosis of stimulation and FOD should be based on arousal. Structural or with vaginal other physical abnormalities must be penetration. there is either lack disorder following a normal sexual difficulty. and substance abuse . There is variable interferes with sexual ture of the outer involuntary pelvic muscle contraction. Criterion Aa Consensus confer. or absence of intensity of orgasmic sensations or exhibit wide variability in attaining orgasm markedly delay of orgasms from any the type or intensity of following kind of stimulation stimulation that triggers sufficient sexual orgasm. and anticipation/ that interferes fear/experience of pain. intercourse third of the vagina (phobic) avoidance. or severe d It is recommended that the following three classes of specifiers are included and considered when making the diagnosis: 1. moderate. Current interpersonal difficulties.1  (continued) Revised definitions from AFUD/AUAF DSM-IV (TR). mild. markedly diminished (FOD) excitement phase. past interpersonal relationships. International Consensus Committee [18]b ence 2000 [19] 2003c. d [21] Female Persistent or recurrent delay Persistent or Despite the self-report of high sexual orgasmic in.

life events/phases. Copied with permission from during the experience. women’s sexual interest. and fact that these entities typically are due to differ. the committee suggested addition consisted of an international group of clinicians of the categories: genital sexual arousal disorder. ANS auto- desire may or may not be present initially: it is triggered nomic nervous system. included sexual motivation as a normative part of which shows several motivations to be sexual. As does not always strongly correlate with subjective with the first consensus conference the panel arousal [22–24]. not necessarily initiated by intrinsic was renamed “women’s sexual interest/desire dis- physical sexual desire. 8. emphasizing that desire and where arousal can occur before recognition is not necessarily manifested by spontaneous sex- of desire. The definition of vaginismus was also changed tions of FSD as displayed in Table 8. and academics from several different disciplines subjective sexual arousal disorder and combined within sexual medicine [21].2  Circular response cycle of overlapping phases: comes influence future sexual motivation. They reviewed the genital and subjective sexual arousal disorders [21]. the lack of specificity of ual fantasies or thoughts [8]. On the basis of this it also sexual meaning. In this model women’s order” reflecting the circular model where it is sug- sexual response is more based on willingness to gested that many women engage in sexual activity find or be receptive to sexual stimuli. 2: Basson [42] she describes a ­circular model and a sexual First hypoactive sexual desire disorder (HSDD) response. significantly as it was found that there is no . Giraldi Fig. Lippincott Williams & Wilkins from Fig. ferent interventions. function is viewed in the context of these factors. contextual factors and suggested that the sexual ent causes and dysfunction in these requires dif. Desire is a for other reasons than intrinsic physical desire as part of arousal triggered by stimuli that has a described above. relationship duration.98 A. literature and suggested new and revised defini. The sexual and nonsexual out.1. Furthermore. a second Another considerable change was in the defini- consensus conference was assembled by the tions of female sexual arousal disorders (FSAD). Furthermore the new the various presentations of arousal was viewed definitions acknowledged that there are fluctua- as problematic. Consequently. since arousal can be described as tions in sexual desire and these are influenced by genital and/or subjective/mental as well as the age. Sexual Health Council of the American On the basis of the observations that genital arousal Foundation of Urological Diseases in 2003. This leads to the circular model.

aversion disorder. and with/without FSD) may has subsequently been changed to persistent endorse different models and the women may genital arousal disorder (PGAD) and many studies change in how they regard their sexual response have tried to describe its aetiology and character. it has been advocated category of arousal disorders based on clinical that one single model may not adequately experience. If describing dysfunction per se. It is rather a reflexive. over time. of reviewing the existing DSM definitions. However. the future challenges istics [27–29]. The name of the disorder pausal status. Sand & order (PASD). thereby not only relating it to refined view of women’s sexual function and intercourse [21]. meno- and intrusive [25. describe all women’s’ sexual response. clinical practice and other settings they and outcome. between a description based on Masters & sistent vaginal and clitoral arousal in the absence Johnson. recommendations of new definitions of FSD. Despite the fact that the new suggested that the fear was towards any attempt definitions provide us with a more specific and to insert an object. In addition it was previous definitions. an equal of sexual desire and which do not subside with number of women chose each model [36]. Kaplan. This condition describes a group Fischer reported that when asked to choose of women who complain of excessive and per. In the revision process. of the women’s sexual response cycle and the involuntary contraction of the pelvic muscles in fact that they were more evidence-based than addition to the thigh muscles. the prevalence of any given dysfunction will inevitably be very high in most populations. .2. It is also to be noted that both consensus defi- lined in Table 8. of Diseases (ICD-10). ent ways women experience their sexuality over the consensus committee recommended that a lifespan. 26]. the still need to be adapted by the DSM or World importance of distress when describing women’s Health Organization’s International Classification sexual problems has been shown to be of signifi. The DSM-V is expected to be [30–32]. During the last several years. This group has published their definitions preliminary recom- DSM-V a Suggestion for New mendations on sexual desire disorder. pain disorder. cant importance when describing FSD in epide- miological studies. three classes of specifiers are included as out. they may not fully reflect women’s Finally the consensus group suggested a new sexual response. and orgasmic disorder as outlined in Table 8. The feelings are unwanted Women with different characteristics (age. one or more orgasms. namely persistent sexual arousal dis. will be in defining FSD embracing all the differ- In addition to these new suggestions for FSD. The The two consensus definitions are certainly an group is suggesting extensive changes in their improvement compared to earlier definitions. arousal Definitions disorder.1 and that distress be measured nitions only remain recommendations for new as it is an important descriptor of the disorder definitions. or Basson’s models. as DSM-V demonstrated by several epidemiological studies reporting the prevalence of FSD to be as high A revised version of the DSM system is under as  55–60% in the general female population consideration. research has shown that finished in 2013. Even though they are used in and has implications for treatment motivation research. a inclusion of sexual distress in the definitions of working group on Sexual and Gender Identity FSD results in a lower prevalence of 15–20% in Disorders has been established with the purpose the general female population [33–35].8  Classifying Female Sexual Dysfunction 99 evidence for the belief that the condition is caused The major advance is the inclusion of the model by spasms of vaginal muscle. Consequently. dysfunction. Recently. reviewing the literature and introduce revised evidence-based definitions.

Lifelong or acquired arousal at least 6 months duration as causes 2.g. Absence of/reduced genital factors (e.g.g. poor communica- and is nor receptive to a tion.g. verbal. Cultural/religious 6. etc. relationship discord. visual. inhibition related to prohibition against sexual activity) 8. poor body image. No initiation of sexual activity (e.g. Individual vulnerability 75% or more of sexual factors (e. inhibition and/or nongenital physical related to prohibition changes during sexual activity against sexual activity) (on at least 75% or more of 7. Markedly reduced intensity of and be or (partner’s sexual orgasmic sensations experienced on interper. Delay in.100 A. Absence of or reduced sexual in desire for sexual excitement/pleasure during activity) sexual activity (on at least 5. discrepancies 4. With concomitant sexual activity problems in sexual interest/sexual arousal 5. Cultural/religious factors (e.g. experience) written. Lifelong or acquired orgasmic symptoms: have been causes 2. Partner factors arousability 1.g. poor communica- tion. problems.g.2  Suggested new definitions of female sexual dysfunction in the DSM-V diagnostic manual [37–41] Criteria A Criteria B Criteria C Specifiers Sexual interest/ Lack of sexual interest/arousal of The disturbance 1. discrepancies in desire for sexual activity) 6. Absence of/reduced sexual/ health status) erotic thoughts or fantasies 4. Individual vulnerability factors (e.) 6. Giraldi Table 8. Relationship factors 3. poor body 5. partners 75% or more sonal health status) occasions of difficulty 4. relationship partner’s attempts to initiate discord. depression encounters) or anxiety. Relationship factors (e. illness/medications) (continued) . Partner factors 2. sexual encounters) illness/medications) Sexual aversion See text for details disorder Female At least one of the two following Symptom(s) must The problem 1. Generalized or disorder (or manifested by at least four of clinically situational sexual the following indicators: significant 3. history of abuse sexual/erotic stimulus (e. partner’s 2.g. Generalized or disorder 1. Desire is not triggered by any image. or absence of present for at marked situational (FOD) orgasm least 6 months distress 3. Medical factor (e. Medical factors (e. history of abuse experience) 7. depression or anxiety. Absence of/reduced interest in distress or (partner’s sexual disorder) sexual activity impairment problems.

2.2. Inability to have vaginal interpersonal endometriosis) intercourse/penetration on at difficulty least 50% of attempts 2. and and the lack of epidemiological studies. recommendation is trying to de-emphasize the . As it can be seen from Table 8. the disorder needs to cause clinically signi­ option based on the lack of epidemiological data ficant distress (B criterion) and finally they and the overlap with specific phobia. on the findings that some women with vaginis- est/arousal disorder.g. The group sees this as the least desirable tion. they try to cover Option 3 is to keep SAD in the DSM-V as a all aspects of desire (spontaneous and receptive sexual dysfunction. On the a C criterion which includes distress and finally basis of this the group suggests three options for specifiers [40] as described in Table  8. sexual inter. Marked tensing or tightning of the pelvic floor muscles during attempted vaginal intercourse/penetration on at least 50% of occasions Sexual Desire and Arousal Disorders Option 1 is to remove SAD from DSM-V and expand the definition of vaginismus to include The group suggests that the diagnoses HSDD and women with sexual aversion [39]. One major problem for the recommendations for a B criterion that establishes a time period of the SAD is the relative few cases of SAD published dysfunction and a frequency of occurrence. Marked fear of vaginal intercourse/penetration or of genitor-pelvic pain during intercourse/penetration on at least 50% of vaginal intercourse/penetration attempts 4. They base their recommen.8  Classifying Female Sexual Dysfunction 101 Table 8.2. 38]. dation on some empirical research suggesting a Option 2 is to remove SAD and make the rec- lack of differentiation between sexual desire and ommendation that cases of genital contact pho- (subjective) arousal in women and the high degree bia are captured under the diagnosis of specific of overlap between FSAD and HSDD [37. This is based FSAD are merged into one diagnose. lichen disorder least one of the following distress or sclerosis. Marked genitor-pelvic pain during at least 50% of vaginal intercourse/penetration attempts 3. despite the lack of empirical desire) in the new definition. mus experience aversion to sexual activity. recommend that the disorder is further described using specifiers as listed in Table 8. phobia in another section of DSM-V. The the DSM-V definition.2  (continued) Criteria A Criteria B Criteria C Specifiers Genito-pelvic See text for further details pain/ Persistent or recurrent difficulties The disturbance With a general medical penetration for 6 months or more with at causes marked condition (e. data. In the recommenda. 1. Female Orgasmic Disorder (FOD) Sexual Aversion Disorder (SAD) The group recommends that FOD is character- ized by an A criterion that describes the orgasm.

In: Lue TF. 7. Davis constantly changing. It should be noted that suggestions for new definitions in the future they also underline that both the physiological DSM-V will be accepted remains unknown. Dudley E. Whipple B. 1st ed. Alexander J. editors. 2004. Classification and diagnosis of female used to describe women’s sexual response are sexual disorders. suggest that dyspareunia is a sexual dysfunction 2. Traish A. 1st ed. Dennerstein L. genito-pelvic pain/penetration disorder. Empty nest or revolving door? A prospective study of women’s and state that: “the pain is not sexual. Maturitas. they argue that the sub. function is being published which hopefully will Washington. Classification. Kamper- As it can be seen from the above overview defini. orgasm. Lewis RW. It is evident that today SR. diagnosis and treatment. Buvat J.102 A. 2004. Leiblum S. 305–14. Fortunately. In: Goldstein I. Dennerstein L. They 5. symptoms and the meno- functions. statistical manual of mental disorders. p.23(2):147–57. Giraldi A. major changes of the definitions of sexual pain disorders and suggests three different options [41]: References Option 1 is to classify dyspareunia together with pain disorders instead of with sexual dys. J Sex Med. Graziottin A. as and the subjective changes experienced by the they are only suggestions and at the present time women during orgasm vary significantly. it should be recognized that the basic domains of desire. physiologi- jective experience is the reason why women seek cal. arousal.4(1):47–56. Standard practice in sexual medicine. Fugl-Meyer KS. Bosch R. Eplov L. population- suggested on the basis that the original separa- based study. tions of women’s sexual problems and the models 8. However. Lehert P. Psychol Med. Dennerstein L. secondly. Sexual Conclusion medicine.32(3):545–50. Sexual dysfunctions in men and women. Dennerstein L. Alexander JL. Davidsen M. and. 2nd ed. Giraldi A. Lehert P. vaginismus and dyspareunia into one. Montorsi F. Diagnostic and in the field of women’s sexual function and dys. to understanding women’s health experiences: a cross-cultural comparison of women aged 20 to 70 including dyspareunia and vaginismus. editors. base this new definition on an A criterion describ. using specifiers [41] as outlined in Table 8. In: Porst H. 1952. p. Garde K. they are debated intensively. Jorgensen F. 2007.2. and ­contextual factors treatment for orgasm problems and not the lack that influence women’s sexuality. Khoury S. Leiblum S. p. 2006. 1. 6. leaving and re-entering the home. 37–72. 1st ed. Basson R. Modeling mid-aged wom- en’s sexual functioning: a prospective. Paris: Health Publications. 2006. London: Taylor & Francis. J Sex Marital Ther. social. Menopause. Dennerstein L. tion of the two disorders was not empirically 4. et  al. based [41]. editors. Option 2 is to collapse the two categories of 2002. DC: American Psychiatric Press. .30(3):173–83. Koochaki PE. Whether the of physiological changes. Rosen R. Study. Women’s sexual function and changes in the definitions must be evidence dysfunction. Guthrie J. DSM-I. Graziottin A. and pain will undoubtedly Dyspareunia continue to make up the foundation of our clas- sifications of FSD combined with a measurement In their recommendations the group suggests of distress. interpersonal.14(4):688–96. an increasing body of research 9. the sex is quality of life in midlife during the phase of children painful” [41]. and epidemiology of sex- ual dysfunction. Meston C. Giraldi physiological aspects of orgasm as they find the enable us to make more accurate and clinically evidence of distinct physiological changes to be relevant definitions of FSD clarifying and adding variable. based. named years. 1996. They underline the lack of evidence to pausal transition. This is 3. etiology and key issues in ing the dysfunction and a B criterion which is the female sexual disorders. Definitions. Giuliano F. American Psychiatric Association. classification. new knowledge to the psychological. 323–30. Oxford: distress criterion and finally further diagnosing Blackwell. A symptomatic approach Option 3 is the suggestion of a new category. 2007. Well-being. Sexual desire in a nationally representa- tive Danish population.

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caveats seriously question the theoretical A recent study on frequency of sexual fantasies. partner whose desire was more similar to hers. Rellini (*) sexual activities. the DSM-IV-TR [1] diagnosis and/or a lack of sexual fantasies that cause relies on reports of distress caused by the low marked distress and/or interpersonal difficulties desire. Golden Keywords  Desire • libido • HSDD • question. sexual desire has been concep- tualized as the motivating mechanism behind A. © Springer Science+Business Media. causing relational distress. individuals who desire sex 3 times a want” more sex. if old report low sexual desire. desire can be identified and reliably assessed. if a woman is in a relationship because many individuals are not alarmed by with a partner with a much greater level of sexual low levels of sexual desire. VT.1007/978-1-60761-916-1_9. desire than hers and the discrepancy in desire is logical study conducted in Australia demon. This diagnosis is intended to include only als who desire sex once a year and are content individuals who experience dissatisfaction with with their levels of sexual desire and sexual their low levels of sexual desire. while women with low levels of week. survival of the species. Mulhall et al. Farmer. These tions in levels of sexual desire in women. assumption that “abnormal” levels of sexual which is an aspect of sexual desire. on average. an epidemio. USA ing experience of inhibited sexual desire can J. Nevertheless. Melissa A. Current Clinical Urology. To add to the confu- will indicate no bother or concerns with the fre. it is possible that individu- [1]. the DSM-IV-TR [1] indicates that a diag- quency of their sexual desire. on average. women Diagnosis experience two sexual fantasies per day and the Hypoactive Sexual Desire Disorder (HSDD) is majority of these fantasies are activated by out- diagnosed when an individual indicates persis. Because of this great variance tent or recurrent blunted levels of sexual desire between women. 105 DOI 10. but only 16% report the same woman were in a relationship with a distress caused by the low sexual desire [2]. LLC 2011 . Because critical component of the diagnosis of HSDD of this criterion.). this condition will often report that they “want to Conversely. However. side cues [4]. women experience sexual fantasies naires • FSFI between once-twice per month to once a week [3]. although an older study on the frequency of sexual fantasies reported that. but are distressed by this frequency may sexual desire that do not meet HSDD criteria be diagnosed with HSDD. Indeed. The chronic and distress- Burlington. (eds. reported that. sion.Chapter 9 Hypoactive Sexual Desire Disorder Alessandra H. University of Vermont. and Gale H. Cancer and Sexual Health. she would not meet criteria for HSDD. Theoretically. The subjective nosis can be made when the low levels of sexual experience of distress caused by low desire is a desire cause interpersonal difficulties. she would neverthe- strated that 32% of women who are 20–70 years less receive a diagnosis for HSDD. Women with activity may not be diagnosed with HSDD.H.P. Rellini. Few studies have empirically evaluated varia. This impetus is central to the Department of Psychology.

For example. is likely to erode the relationship. women report they no longer express changes in sexual health is an important aspect affection or touch their partners. surgery. each not knowing how to move out of their preferred sexual stance. medication. or reducing sexual dysfunction by simply educat- experience guilt for withholding an important ing their patients about sexual desire changes part of a satisfying relationship and harbor feel. commonly cited reasons for treatment discon- The guilt of “starting what they cannot finish” tinuation even for conditions that cause high lev- prevents them from exchanging innocent forms els of emotional distress. orgasm. 42% of men and 15% of women discontinue the quences beyond the sexual realm. distress caused by changes in sexual desire can tion as compared to couples with higher frequen. such as holding hands. such as hormonal contraceptives. engaging in sex without feeling desire. or psychiatric condition. and directionality of this relationship remains debated illnesses can affect sexual desire. ings of inadequacy and poor self-esteem – all of surgery. . Rellini et al. Having realistic expectations for desire. For example. such as depression. kiss. In the long term. Moreover. medication over perceived beliefs of sexual studies have shown that couples reporting low adverse effects [8]. while the partner with little or no sexual desire feels guilt and shame. Women who experience a loss of time can be incorporated in a preventive health sexual desire might be faced with the choice of education or sexual education program. or even changes which could impair mental health. severe personal and relational relationship adjustment and relationship satisfac. els of the sexual cycle. adversely affect quality of life. and resolution. there and promote overall quality of life not only for is often resentment on the part of the partner the patient. Couples are often left to grapple with a cyclical and nonproductive conversation to make Theoretical Models of Sexual Desire a change. Because of that result from life changes such as pregnancy the guilt often associated with inhibited sexual or menopause. information regarding potential levels of personal distress. accurate information about as compared to couples who are satisfied with a changes in sexual desire associated with a treat- low frequency of sexual activities. Indeed. 6]. because and medication doses. Healthcare providers may be instrumental in ulate because they fear losing their partners. be addressed by healthcare providers through cies of physical intimacy [3. were the first to conceptualize the model of the To prevent this dysfunctional cycle where sexual cycle to begin with sexual arousal and HSDD fosters resentment and greater sexual continue with plateau.106 A. However. the simple education of how treatment. research on antidepressants showed that that inhibited sexual desire has relational conse. or problems and can also help managing treatment casual touch. By providing [7]. women’s lives. and of affection and this leads to greater distance in for drugs that provide an important function in the relationship. but capit. lead to high dysfunction. When couples ment can help prevent treatment discontinuation experience different levels of sexual desire. with or without professional interven. It has been well documented in the literature Indeed. Masters and Johnson [9] tion. and cause relational changes and shifts in sexual desire over a life- difficulties [5]. It is important to note that the frequency of accurate information to the patients. The HSDD diagnosis is based on the early mod- this cycle.H. treatment-induced they are afraid this would mislead their partners inhibition of sexual desire is one of the most to think they want to engage in sexual activities. the health- sexual activities per se may not be the problem care provider can have a significant impact on and that a decrease in frequency of sexual activi. frequencies of physical intimacy score lower on In summary. but also for her partner. that may be the result of an illness. who has high levels of desire. the prevention of dysfunctional patterns in the ties may cause greater distress in couples whose relationship that can lead to chronic sexual dys- sexual lives are dramatically affected by HSDD functions. of health care that can help prevent sexual desire they often report withholding a hug.

g. According to this model. or to or fantasies is less relevant than information succumb to peer pressure [17]. romantic dinner is no longer feeling sexual desire As noted above. and sexual behaviors may occur in the A third model. a study on premenopausal and menopausal after sexual arousal [11]. without HSDD [14]. an assessment of ual desire proposed by Basson argues that sponta- how a woman used to respond to a sexual cue neous sexual desire is not the norm in women. However. symptoms. she anticipates.. The debate is centered on whether responses of a second group of 874 women of desire and sexual arousal are distinct experi. desire continues to be understood as a activity are the sources of spontaneous motiva. Kaplan’s model is considered grouped into four cue types based on the controversial. has found support in a recent empirical study inal theoretical model by adding sexual desire in [13]. Therefore. prior to sexual ent cues of sexual desire that were analytically arousal).. for instance. tional and physical rewards resulting from sexual Today. and empirical evidence for this model provides lation. sexual desire aside. according to this model. absence of desire. The distinction changes in the cues that activate sexual desire. In this model (often women showed that individuals with HSDD called the Circular Model). originally by Kaplan (the model proposing that desire developed through extensive clinical experience. The emo. To date. the theoretical model for sex- after similar activities. motivating force to engage in activities that can tion for later sexual activities.g. for riences of sexual desire provide more clinically example. proposed by Levine [12]. to ensure theory. sexual desire the treatment of sexual desire is contingent to the does not always directly precede the behavior it experience of satisfying sexual activities. The four ana- ences.. From a behav- activities that fail to provide satisfying physical ioral perspective. An material. romantic experiences. between sexual desire and frequency of sexual For example. sexual response posits that desire is experienced Later. oriented behavior [16]. the other hand. motivation is the driving force and emotional rewards may diminish sexual behind the initiation and maintenance of goal- desire in women [11]. lower- experiences. A group of 50 women identified 125 differ- the beginning of the cycle (i. always precedes sexual arousal) or the model . The next step will be to establish whether sexual stimulation. niscent of the 11 sexual cues that Levine A more recently proposed model of female identified based on his clinical observations. 17–72 years old (Table  9. Thus. This model. women may not act on their sexual desire. social norms or fear of pregnancy. 13).1. seeing a partner acting competently) is empirical study that asked women whether they more important than the assessment of overall identified more strongly with the model proposed frequency of sexual thoughts. motivates. sexual lead to sexual satisfaction [14]. but (e. a specific scent. the woman internalizes the desire ing the threshold of desire activation in the for future sexual activities that. Once the sexual activity has increasing the variety of sexual cues and modu- led to satisfying emotional and physical sexual lating the sensitivity to sexual cues (e. a clinician behaviors connected to desire [3] makes the would benefit from assessing whether a woman assessment of desire more complicated than it who used to experience sexual desire after a may initially appear. with desire always preceding sexual lytically derived types of sexual cues are remi- arousal. it is proposed that the endorsed significantly fewer cues than women woman experiences sexual arousal after her part. The sensation of sexual arousal leads to unique support for the validity of perceived sex- positive associations with sexual behavior and ual cues as meaningful contributing factors of these associations motivate desire for further HSDD. erotic rather it is the product of sexual arousal.e. an overall frequency of sexual thoughts the fidelity of a mate. to spite someone. There are a number of reasons emphasizes that variations in individuals’ expe. presence of a sexual cue) could alleviate HSDD will lead to similar sexual rewards. According to Levine’s engage in sexual activities.9  Hypoactive Sexual Desire Disorder 107 Kaplan [10] revised Masters and Johnson’s orig. women may ual thoughts or fantasies. On relevant information than just frequency of sex. The combination of clinical ner approached her with sexual cues and stimu.

g.108 A. Presenting the patient with oping sexual dysfunction and (2) whether women’s this option opens the opportunity for education on perceptions of their sexual response cycle can different perspectives of sexuality and provides a .. perfume/cologne. or erection Asking for or anticipating sexual activity Hearing your partner tell you that he or she fantasized about you Having a sexual fantasy (e.g.g... Future studies are cians may be to present both models to a patient needed to assess whether (1) the tendency to iden.g. sports) Seeing someone act confidently Seeing/talking with someone intelligent Flirting with someone or having someone flirt with you Romantic/implicit Whispering into your partner’s ear/having your partner whisper into your ear Dancing closely Watching a sunset Having a romantic dinner with a partner Watching a romantic movie Being in a hot tub Touching your partner’s hair or face Giving or receiving a massage Laughing with a romantic partner Smelling pleasant scents (e..g. A useful tool for clini- more with the former [18]. shampoo. proposed by Basson found that women with a change as their sexual functioning develops and sexual dysfunction identified more with the latter changes over time. aftershave) From McCall and Meston [13]. having a sexual dream.1  Type of cues of sexual desire Type of cues Examples of cues Emotional bonding Feeling a sense of love with a partner Feeling a sense of security in your relationship Your partner is supportive of you Your partner does “special” or “loving” things for you Feeling a sense of commitment from a partner Your partner expresses interest in hearing about you Talking about the future with your partner Feeling protected by a partner Experiencing emotional closeness with a partner Feeling protective of a partner Explicit/erotic Watching an erotic movie Reading about sexual activity (e. pornographic magazine) Watching or listening to other people engaged in sexual behavior/activity Talking about sexual activity or “talking dirty” Watching a strip tease Sensing your own or your partner’s wetness. Rellini et al. and ask her to identify the model that reflects her tify with a specific model can be a factor in devel. personal experience.H. lubrication. Table 9. daydreaming) You experience genital sensations (e. Both models are currently and women with no sexual dysfunction identified utilized in clinical settings. increased blood flow to genitals) Visual/proximity Seeing someone who is well dressed or “has class” Seeing/talking with someone powerful Being in close proximity with attractive people Seeing/talking with someone famous Seeing a well-toned body Seeing/talking with someone wealthy Watching someone engage in physical activities (e..

exter. Among the chapter. Although norms HSDD assessment. If Individuals scoring positive on the screener. a lifelong issue. In other words. There opportunity to assess whether the low levels of are two such screeners currently available: the desire are lifelong. a crisis caused by Both screeners exhibit good sensitivity and spec. goals. Although an in-depth explanation of this useful to set goals for treatment and to track pressing discourse is beyond the scope of this treatment-related improvements. supports the idea that women’s sexual with low desire. Establishing the definition Questionnaires assessing distress and satis- of normal sexual desire as internally vs. the Sexual Satisfaction Scale for Women utility of different treatment modalities and the [24] is one that captures both satisfaction and aspects of desire to include in a preliminary distress with sexual functioning. the debate on whether desire precedes severity of sexual symptoms. Clinical cutoffs based on popu- desire is naturally derived from outside cues or is lation norms allow clinicians to quickly assess reactive in nature. the product of a slow decline. Conversely. or cal. thoughts or fantasies. Although these and may not necessarily be based on outside questionnaires cannot be a substitute for a thor- cues. this model the severity of the symptoms in relation to the questions the importance of spontaneous sexual larger population.2) A more comprehensive sexual health history can uncover important diagnostic information A number of instruments developed for the not fully captured by brief questionnaires. A personal interview also provides an experience problems with sexual desire. Examples of spontaneous sexual desire are ough interview covering the sexual. and the change was sudden. can complete aimed questionnaires that measure In sum. available published measures for sexual satis- ing positions can be useful for understanding the faction. potential etiological factors of low sex- Clinics not specialized in the treatment of sexual ual desire can emerge from an interview that dysfunction can utilize a brief screener of includes questions about the relationship HSDD to identify women who are more likely to dynamic. pro. Measures of distress/satisfaction can also be ment. suggesting clinical and research use for women who may that desire can be activated by internal forces have sexual dysfunctions [21]. life. problem and provide the clinician with popula- posing that sexual desire occurs after sexual tion-based norms on levels of distress associated arousal. For instance. or perhaps a slow ificity. gering event. example. the Female Sexual some women experience sexual desire before Functioning Index [22] and the Sexual Function sexual activities implies that a woman may expe. an understanding of these two conflict. and are not activated by any external adequate measures of severity of the sexual stimulation. faction can be utilized to provide a measure of nally derived determines what is perceived as the impact of the problem on the patient’s daily “abnormal” and thus directs the focus of treat. infidelity. and expectations of treatment. According to a or follows arousal is implicitly a discussion on recent review of 28 questionnaires for female the nature of sexual desire.9  Hypoactive Sexual Desire Disorder 109 theoretical framework to conceptualize sexual indicating interest in greater support in this area. The perspective that sexual functioning [21]. meaning that the instruments are able to decline since menopause can be important fac- correctly identify people with the disorder. other issues can be . for women with and without HSDD are avail- able. therefore it is best used to monitor treat- ment-related improvements. Assessment of HSDD (Table 9. tors in the assessment and treatment of HSDD. psychologi- sexual fantasies that emerge during the day. the circular model. they are the night. Questionnaire [23] were recommended for both rience spontaneous sexual desire. currently the scale lacks cutoffs for clinical levels. symptoms. Hypo­active Sexual Desire Screener [19] and or whether a reduction followed a specific trig- the Decreased Sexual Desire Screener [20]. and medical history of each patient. For assessment of HSDD are available to the public.

since the low desire may be a desire was an antecedent or consequence of the symptom of a larger problem rather than a cir- accompanying sexual dysfunction.g. Desire is both spontaneous desire for sexual activities and    the tendency to respond when a partner initiates sexual activities 2) Assess whether levels of sexual desire are lower than wished by the patient (not necessarily her partner) 3) Assess whether the low level of sexual desire causes distress or bother in the patient (not necessarily her    partner) 4) Investigate whether the levels of desire have always been low (lifelong) or if they were higher at some point   (e. desire and it would be appropriate to treat these Moreover. low levels of sexual ment of HSDD. Rellini et al. .    shame.H. with androgen has been identified as more accurate alcohol or substance use. laboratory exams including female orgasmic disorder. discuss later. including whether of sexual desire.. anxiety disorders. it is common for women with sex- ual arousal dysfunction to experience concurrent low sexual desire. or before a specific event) a) Investigate the circumstances of the event b) Explore the pattern of change (sudden or gradual change) c) Establish the amount of change noticed by the patient 5) Assess the attribution for the low sexual desire by the patient 6) Assess relationship satisfaction. or after the decline in sexual desire may help identifying important Low sexual desire is often observed in people etiological factors to target during treatment. and whether partner’s sexual health is have been linked to impaired levels of sexual playing a role in the low desire of the patient. The most commonly used labo. and diabetes (or both). DHEA-S. during an interview include whether the low conditions resulting in amenorrhea. interviews aid in identifying other conditions before attempting the direct treatment coexisting sexual dysfunction. points of disagreement. experiencing other psychiatric conditions such In addition to clinical interviews. a change in medication. In such cases. and DHEA. in pervious relationship or earlier in current relationship. for example. in concurrence with. and sexual pain disorders. For examples.110 A. low androgens levels. female include an assessment of free testosterone. information on intrapersonal drops in emerged within the romantic relationship. including beliefs that could lead to guilt.2  Topics addressed during a complete assessment of hypoactive sexual desire disorder Topics to target during HSDD assessment 1) Ensure patient understands the definition of desire. laboratory as depression. can be compared to population-based norms. An assessment of medical condi- sexually abusive experience. orders [25–28]. and anxiety explored during an interview. As we will cumscribed and independent condition. Table 9. ability of the couple to communicate emotional material. or as aftermath of a information. desire are commonly reported by women who ratory tests include an assessment of abnormally also experience other types of sexual dysfunction. oligomenor- desire causes personal or interpersonal distress rhea. determining whether the sexual arousal dysfunction occurred Differential Diagnosis prior to. In addition. sexual arousal disorder. Patients’ androgens levels whether the patient experienced a recent illness. polycystic ovarian syndrome.    and power distribution within the couple 7) Determine the major points of life stressors in the patient and her coping style 8) Inquire about relevant past sexual experiences including a history of sexual abuse and childhood trauma    including emotional and physical abuse 9) Assess emotional responses to sex that could affect sexual desire. or whether problems however. Usually. and eating dis- tests can provide useful information for treat. before menopause. Other clinically tions associated with estrogen and androgens meaningful information that can be explored abnormalities can also be useful. before pregnancy.

levels of sexual include loss of sexual desire as part of the vege- desire may have dropped after a series of sexual tative symptoms of this condition. they exploration of potential maintaining factors. in general. the orgasm is the primary dysfunc. For example. very little is known about the coexistence reduction in motivation for sexual activities. As we have discussed above. Thus. For example. From a treatment point of view. and disappointment may overlook example. young college students experiencing an important aspect of her sexual health. known about the importance of treating desire in lems with desire could eventually lead to low relation to other sexual difficulties. interestingly. In occurrence of reduced sexual desire as part of a such a case. factors that desire in the presence of chronic sexual arousal maintain HSDD may be equally (or more) impor. distinction. should be considered two distinct experiences The high coexistence of HSDD and other [29]. the along with the difficulty in reaching orgasm. it is arousal or problems with orgasm and sexual unclear if it is possible to maintain normal sexual pain. Indeed. yet. sadness. treating the desire problem tualized as part of a more generalized loss of alone may not be sufficient. under. experiences difficulties becoming sexually It should be noted that despite the importance aroused or reaching an orgasm is not likely to to ascertain the temporal precedence between experience the physiological pleasure associated HSDD and the other types of sexual dysfunction. Individuals experiences that failed to lead to orgasm. If desire is the motivation to during sexual stimulation. Problems of sexual desire are highly preva- standing the factors that perpetuate the lent in women experiencing clinical depression. also reported reduced interest in engaging in Female sexual arousal disorder and HSDD sexual activities with a partner [30. However. women are not complex sexual or psychological cluster of the only ones confused about the desire-arousal symptoms or whether it is a symptom indepen. guish between problems with arousal. the rela- treating the orgasm without addressing the low tionship between loss of desire and depression desire caused by feelings of anxiety. and desire are listed in Table 9. is poorly researched and quite complex. with sexual activities and this could lead to a to date. whereas subjective sexual arousal force to pursue or engage in gratifying sexual comprises the sensations that women experience experiences [15]. orgasm. These are particularly difficult to distinguish because findings suggest that individuals experiencing women often do not intuitively differentiate major depression do not completely lose interest . depressive episode precludes the diagnosis of tion that subsequently caused the development HSDD because the change in desire is concep- of HSDD. For inadequacy. including sexual activi- experiences. At the same time. desire is defined as the experi- types of sexual dysfunction [22] can be best ence of longing or wanting to engage in sexual understood if we look at desire as a motivating activities. or orgasm problems. dysfunction in the present moment is central to Indeed. motivation and interest. experts dent of other pathology is a requisite part of a are still debating whether desire and arousal complete HSDD diagnosis. the woman may feel a loss of desire ties. tant than initiation factors. therefore. It is of desire and other diagnoses and even less is also possible for the inverse to be true and prob.9  Hypoactive Sexual Desire Disorder 111 Identifying whether HSDD is part of a more arousal from desire. any obstacle to the rewarding aspect of the sex. a woman who they can be quite informative. Although these ual experience. can potentially have an adverse effect they are commonly used in clinical practice and on sexual desire. a depressive symptoms within the clinical levels clear understanding of what started the sexual for major depression reported a strong interest problems needs to be addressed along with the and desire to masturbate. or with motivating mechanisms questions have not been empirically validated. the diagnostic criteria for depression the assessment. Currently. 31].3. Nevertheless. According to the DSM-IV-TR [1]. Therefore. Questions to distin- engage in behaviors that lead to sexual rewards. After with major depression lose interest in many numerous unsuccessful and frustrating sexual pleasurable experiences.

g. hugs. yet modality for treatment as the issue was both some serotonin-norepinephrine reuptake inhibi. it was astoundingly high prevalence of impaired sexual decided that couple therapy would be the best desire associated with these medications. had been postmenopausal for several years depressant medication use and decreased sexual before she sought help. Mary had depressive episodes prior to her itors (SSRIs) as primary culprits for antidepres. She felt confident that without being . another and shared kisses.3  Questions to differentiate between HSDD and other sexual dysfunction If I had a pill that increased your level of sexual arousal (how much your body gets turned on during sexual activities) do you think your desire would increase as well? If I had a pill to increase the frequency and/or the intensity of your orgasms. During specific sample (e. and what was the relationship like during that time? Was there a time when your orgasms were more intense and more frequent than now? If yes.H. couple therapy). sure prevalence of sexual dysfunction in this However. 5-HT2A antagonist. with women on antidepressants being was that after her surgery for uterine cancer. Her primary complaint desire. had no sexual desire. 33]. she psychiatric conditions. have targeted selective serotonin reuptake inhib. and the use of SSRIs. Years of research might affect their sexual relationship. and restricted mation about how the treatments and surgery duration of antidepressant use).2–2. flibanserin. diagnosis of uterine cancer and had not been sant-induced reductions in desire based on the treated. during an initial attempt at vaginal population. by stringent exclusion criteria in most studies They were both very anxious that they might that limit the extrapolation of findings from a never be able to have intercourse again. the problems with sexual desire or the problems with sexual arousal/orgasm? for activities that lead to sexual reward.. For exam- HSDD and depression.e. and a D4 partial her mother had been able to take advantage of agonist) indicate that future antidepressants may them. cific to a subset of sexual activities that include It is also possible that when the depression partners (potentially as an extension of social abates due to psychotherapy (individual and/or isolation often experienced with depression). indeed facilitate levels of desire [34]. The loss not adversely impact sexual desire. The standard critique of studies marriage of 26 years with a husband who was correlating antidepressant use with blunted very supportive and not demanding of sexual desire is that sexual disturbances are part of the contact. no concurrent use of and her husband had not been given any infor- other psychotropic medications. what was your sexual desire then. and touching dancy complicates our ability to accurately mea. This sound critique is overshadowed intercourse. They both were affectionate with one diagnostic criteria for depression and this redun.5 times at greater risk for sexual dysfunc. what was your sexual desire then? [If the individual indicated that she is also experiencing sexual arousal or orgasm problems] What started first. a 5-HT1A of medications that were available and wished agonist. She was in a satisfying tion [32.112 A. would your sexual desire increase as well? Was there a time when it was easier to become sexually aroused than now? If so.. Rellini et al. one another in nonintercourse encounters. she experienced a great deal of pain. Data on mother who was depressed most of her life. no comorbid medical or Mary’s diagnosis and treatment for cancer. Mary brought up tors (SNRIs) show equally dismal rates of the idea of trying antidepressants as she had a reduced desire (see [33] for review). newer antidepressants with highly specific Mary knew a great deal about the current family mechanisms of action (i. then part- To complicate the relationship between nered sexual relationships improve. but may of sexual desire for these women may be spe. Mary was 54-year-old married woman who robust evidence for a relationship between anti. Table 9. she 2. After a thorough evaluation. the literature has shown ple. relational as well as personal.

Biological Factors ual desire is not experienced as distressful by all women. 36. In this Studies case. and relational issues. However. she would be more willing to engage tress in these incidence rates. Although we attempt here to highlight a broader repertoire for sexual expression. and at times. Couple therapy enhanced their ability to of mechanisms that the literature has linked to sex- communicate about sexual issues and to develop ual desire. A few of women report a decrease in sexual desire within studies have found that for women with particu- the prior 5 years [41]. and estrogens is women found that rates are double in the poorly understood. Developmental fluc- The only incidence studies available to date tuations in estrogens and androgens observed were conducted in Finland and Sweden in the early during menopause are associated with a decrease 1990s. it is not possible to deduce [42] and injections [43] can be effective at the actual incidence of HSDD from this study. Prior to the surgery. 39]. larly low levels of androgens. A pelvic Desire physical therapist was suggested for dealing with vaginal pain. these treatments is under investigation and the . based on prior stud- in sexual contact with her husband even if she ies of desire frequency and distress [39]. and between 15 and 34% report that the low desire causes distress [2. for example. androgens. desire is difficult to isolate. tion comes from studies on sexual desire during based studies in Iceland and Morocco [40]. physiological impair- ments to intercourse. increasing sexual desire. a lifelong struggle with depression provided an impairment in her serotonergic system. She felt she would enjoy sex once she and her husband were engaged even if she Factors Implicated with Sexual felt no desire going into the encounter.9  Hypoactive Sexual Desire Disorder 113 depressed. The age trend found in Sweden is com. We have discussed. and building confidence for vaginal contain. the relationship desire increase noticeably. Most of this informa- parable to what has been reported in population. it is undeniable dent of age up until age 50. the menopausal transition. the that sex hormones play an important role in sex- rates of low sexual desire and distress caused by ual desire [30]. the safety of although we would expect reduced reports of dis. she had always been orgasmic and willing to engage in intercourse. these three domains do not manifest regarding sex and allowed them to become a independently from each other. 38. After age 50. their relationship was stable. it is important to note that. roid hormones on desire. may more “intimate team” working together to meet not be distinguishable from one another. The the challenge of “good enough sex” after cancer impact of each separate variable on low sexual [35]. While the independent effect of biological. Due to the lack of informa. From a biological perspective. an androgen patch tion on levels of distress. However. 50–60-year-old cohort compared to younger there is persuasive data on the impact of sex ste- women. Population-based studies indicate that 29–39% of women report low or no sexual desire in the previous month [2. 37]. how in Mary’s case. Rates of low sexual desire are indepen. These studies found between 40 and 45% in sexual desire (for a review see 30). Cancer provided additional HSDD Prevalence in Epidemiological psychological and physiological problems. The complexity of HSDD is reflected in the myriad ment. pelvic floor strengthening. the depression and cancer worked together to provide low sexual desire. These rates elucidating that low sex. psychological. in their ability to communicate about expectations the patient. did not feel much desire. therapy enhanced and relational factors. Even with this lack of clarity. A study of Swedish between desire.

sexual behavior is chotics (most of which antagonize D2 receptors) tightly connected to the estrous cycle and depri. a lack of sex- Characteristics of estrogen receptors are also ual desire can signal a problem in the area of psy- key in understanding the modulation of circulat.H. Thus. ther evidence for the role of dopamine in the Estrogens levels are also associated with sex. and conversely. oid antagonists prevent female rats from learn. The regulation of estrogen recep. being to focus on self preservation over any other ied neurotransmitters in the modulation of sexual activity. learned sexual with mood or anxiety disorders) may show a preferences and desire for access to sexually reduction in sexual function that is not warranted. that has been associated with low logical maladjustment can adversely impact mul- sexual desire [46]. estrogen does not have such a clear effect on sexual desire. Similarly. increases levels of sexual desire. (a 5-HT1A agonist. are disrupted. Dopamine and practical for people perceiving threat to their well- endogenous opioids are some of the most stud. In women. increasing they have previously learned to pair with sexual androgen levels in women not experiencing rewards [15]. estrogen and testosterone. and psycho- gen per se. 50% were diagnosed with a tors is modulated by progesterone and androgens. rather than hormones that directly modu. Normal Psychological Factors fluctuations in estrogens during the menstrual cycle have been linked with fluctuations with Psychological well-being is highly correlated desire in some studies. In states where the individual is strug- desire [47]. and a itate the normal fluctuations and peaks in sexual D4 partial agonist). As a result. This evidence provides an indirect indication Female rats given dopamine antagonists will not that abnormal decreases in androgen levels can express sexual preferences for specific cues that negatively impact desire. estrogen antagonists) leads to the complete ces- sation of receptive behavior in the female rat [15].e. positive effects of such treatments are modest [44]. gling with a threat to safety. also report lower . a dis- antagonists also impair the expression of sexual order that disrupts primary physiological needs desire by altering the salience of sexual cues and including sleep and eating. However. providing fur- late desire. the suppression of sexual desire dur- essential motivating mechanisms to engage in ing states when the individual is fighting for sur- specific behavior. An organ- Therefore. indicating that when sexual activities sors in their environment and may show an are not paired with opioid release. antipsy- ual desire. other neurotransmitters impli. with sexual desire. it is often the combination of low ism functions according to a hierarchy of needs. It is therefore likely to affect sexual desire. seeking sex therapy. as first proposed by Maslow [50]. physiological needs. In animal studies. but not others [30]. individuals are not perceived. coexisting psychiatric diagnosis [49]. tiple levels of needs. rather than low estro. desire in premenopausal women. the behavioral response to rewarding stimuli. Rellini et al. vival ensures that reproduction occurs when cated with the general motivation system are energy and resources are available. flibanserin are better conceptualized as hormones that facil. Indeed.114 A.. chological adjustment. however. Dopamine Individuals suffering from depression. Animal studies have found that opi. 5-HT2A antagonist. In a study of 126 women ing estrogen. From an evolutionary Given that sexual desire is comprised of perspective. indi- ing that specific stimuli can lead to sexual viduals who tend to be overly sensitive to stres- satiation. androgens aminergic and serotinergic systems. sexual rewards exaggerated response to stressors (i. modulation of sexual desire. are notorious for reducing the appreciation of vation of estrogen (via ovariectomy or the use of pleasure [48]. intact males will not be expressed [15]. such as procreation. Recent studies on humans have androgen deprivation is unlikely to lead to an found that a compound that acts on both the dop- increase in sexual desire [45].

This hypoth. a pathway associated ner can affect a woman’s sexuality. a woman’s desire to engage in the multitude of systems affected by cancer and sexual activities may be affected by her sense of cancer treatment. Data from with emotional processes and motivation. it is feasible that impairment in the sexual dysfunction and the health of the part- the mesocortical pathway. Women with the relationship is also important for treatment HSDD are indeed more likely to have a history outcome. Quality of no depressive symptoms [51]. a gynecological or breast cancer. States of food deprivation affect this focused on nongynecological cancers (including system and send signals that the organism is in a lung.9  Hypoactive Sexual Desire Disorder 115 levels of sexual desire compared to people with overall relationship satisfaction [7]. and rectal cancers). Alternatively. esis is largely speculatory at this point given the While the initial studies on breast cancer were lack of information available on sexual function mostly focused on the potential effect of mastec- in women with eating disorders. other psychopathologies often accom. Resources are the majority of the information currently avail- released in the body. we will discuss the effects of closeness and intimacy with her partner and her cancer and its treatment on the three components . physical attraction between partners were the panied by inhibition of sexual desire include first and third most commonly reported factors schizophrenia and anorexia nervosa. PsychInfo. 57] painted a dif- ferent picture and provided evidence that side effects of treatment (and especially radiother- Relationship apy) on sexual desire are more debilitating than the psychological effects caused by mastectomy. The rela. and PubMed databases for responsible for facilitating the release of resources articles published in the past 50 years on cancer to key organs involved in the fight and flight and sexual desire. which enters a survival state. only a handful of articles response. the antipsychotics used to treat schizophrenia may depress appreciation of sexual reward. and a relationship. at this point. tomy on women’s body image and therefore on her sexuality. Therefore. stood as limited to these specific types of cancer tion system for functions not necessarily linked populations as it is unclear whether these results to immediate survival is shut down. tionship between schizophrenia and sexual respectively. When sexual desire occurs within the context of Because of the multifaceted nature of desire. state of potential starvation. From a theoretical In addition to the quality of the relationship. able on cancer and sexual desire must be under- It is plausible that during this state. point of view. pituitary. However. A review of clinical outcome studies of major depression compared to women with for desire [53] found that overall quality of the no HSDD [52]. The association between anorexia nervosa and The majority of the studies that investigated sex- desire may be implicated with the impairment in ual function in cancer survivors focused on the hypothalamus-pituitary-adrenal (HPA) axis. In addition to mood and anxiety couple’s nonsexual relationship and degree of disorders. 55]. would apply to other forms of cancer. associated with positive treatment outcome. thereby Cancer blunting sexual desire. sexual women was associated with lower sexual the lack of empirical studies on this topic and desire functioning and greater overall sexual the complexity of both schizophrenia and sexual dysfunction in women [54. In our review of system closely connected with stress that is Medline. the motiva. may longitudinal and cross-sectional studies found be also responsible for the low level of sexual that poor health in the male partners of hetero- desire in patients with schizophrenia. desire is poorly understood. later studies [56. desire prevent a clear acceptance or rejection of such hypothesis.

After 6 Psychological Factors months. a measure of desire (31%) are comparable to patients with androgen that is more closely associated with gynecological cancer [59]. existential relationship. problematic social support. We will now look individually at main factors review of desire: biological. sion are difficult to tease apart from physiologi- cal and treatment-related effects of cancer treatment (e. Psychological. coma cancer. intrasellar tumors were positively associated cervical. 70% reported improvement after comply- Depression is a common consequence of a life- ing with treatment recommendations. Biological Prevalence of Low Desire and HSDD in Cancer Patients The only data available on the direct biological effects of cancer on sexual desire come from The prevalence of desire problems in cancer studies on cancer affecting the HPA axis. Sexual desire may be diminished follow- Relational ing chronic depression. researchers found that the best predictors metabolic changes associated with cancer and of sexual function and satisfaction postbreast its  treatment. with loss of sexual desire [62]. including chemo. that arise in individuals suffering from cancer tional well-being. populations is elevated compared to national According to a study on 53 women with pituitary averages. anxiety related to death. levels of sexual desire were inhibited gynecological cancer. that women were both interested in receiving between 15 and 40% of individuals with cancer support for the side effects on sexuality and dem- will experience depression or anxiety during the onstrated the motivation to follow through with course of their illness [63]. which is associated with  altered HPA axis function and persistent Based on data from 817 women who had under. 56% reported low levels or  desire was lacking in approximately 80% of sexual desire and 35% of the 20 women of  patients [62]. immune activation [64]. and desire. and sar. 43% complained of HSDD and asked for clinical recommendations [60]. changes in appetite and weight). emo. In a sample of 20 women treated for tumors. Symptoms of depres- such suggestions. Levels of sexual desire were had both depression and sexual dysfunction neither correlated with hyperprolactinemia nor [58]. which. and therapy. Both clinical depression and treatment- Direct Effects of Cancer on HSDD: related depressive symptoms may impair sexual Biological. For patients with breast cancer.H. and in sexual satisfaction in breast cancer survivors tolerance of prolonged treatment and cancer . Indeed. body image.. relational. vaginal. but age and presence of In a sample of 96 patients treated for ovarian. Rellini et al. the rates with serum testosterone (although no data was of women reporting interferences with sexual presented on free testosterone. levels of sexual desire). indicating threatening condition like cancer. may gone breast cancer treatment. endometrial. of sexual desire preciously identified in our [61].116 A. fatigue. Prominent psychological issues cancer are: absence of vaginal dryness. of all patients requesting clinical consul- tation. adoption of poor cop- These variables accounted for 33% of variance ing  strategies. in turn. quality of the include feelings of grief and loss. compound the broad immune. and impacting sexual desire with the understanding psychological. that these factors often act in orchestration and not independently.g. and partner’s sexual problems. vulvar. endocrine.

framework on which the individual forms a sense Receiving a life-threatening cancer diagnosis of self that is coherent across time and situations. ated with treatment. chotherapy. self as embarrassed and sexually conservative. Negative Alternatively. may therefore be good candidates for therapy. Guilt is more commonly expe. leaving the patient to deal macy. can motivate a number of fears that directly. fear that the disease are at higher risk for later sexual problems. thereby causing even . Andersen and coworkers [66–68] the patient and her spouse/partner are important found that endorsing adjectives that describe the steps for the healthcare provider interested in pre. supportive relationships are associated of cancer and this may lead to the feeling that with better health outcomes for cancer survivors. upset the relationship. In a series of studies on sexual before the surgery) and establishing a rapport with self-schemas. At their basic level. The perception a person has of her behavior can lead to physically and psychologi- self (self-schemas) provides a blueprint on how cally painful sexual experiences. it is possible that the sexual affect caused by fear and guilt acts as a motiva. problems [69]. who will reoccur. Assessing a patient’s sexual his. romantic. A life-threatening diagnosis can change a roman- ated with cancer can have a direct effect on tic relationship in a variety of ways. prior to the activities despite a lack of sexual desire. diagnosis will likely increase the sense of inti- rienced among women with cervical cancer macy and commitment between the partners. the sexual activities. they are of particular interest for treat- family system. Such diagnosis [67]. This avoidance can counterintuitively lead with her medical condition and the relationship to the strengthening of these negative emotions. or losing the ability to procreate.e. For example. Although schemas are stable features of our well. and thus a promiscuous sexual history both the individual and the prognosis of treatment. Patients who feel compelled to The psychological effects of cancer on the please their partners by trying to maintain their sexual desire of a woman are moderated by her prediagnostic sexual life may engage in sexual view of herself as a sexual being. ment since they can be modified through psy- tory and her baseline sexual functioning (i. inhibit sexual desire. open. because this form of cancer is linked to genital These relationships can have a positive effect on herpes. a cancer diagnosis has a profound impact on and how her sexuality changes during treatment not just the patient. and not endorsing adjectives such as passionate. In the case of gynecological loving.. The combination of the stress caused Schemas emerge from past experiences and the by this life-threatening condition and cognitive meaning that the individual gives to these experi- vulnerabilities that may lead to depression can ences. contaminating others. predicted a cancer. venting or containing HSDD symptoms associ. the wish to reject physical contact. the fear of damaging one’s body. and direct. but their spouse/partner as [66]. sexual function since it can activate avoidance of if a partner or spouse is supportive and caring. may be likely among individuals with this type Indeed. schemas provide a affect sexual desire. and it is likely to create ripples in the entire identity. or Studies have indeed found that a woman’s sexual indirectly. dysfunction secondary to cancer treatment may tor to avoid sexual activities or any form of inti. Schultz and van de Wiel [65] listed sexual self-schemas conducted at the time of common feelings evoked by gynecological cancer diagnosis can aid in identifying individuals who that affect sexual desire: guilt. she caused (and deserves) the disease. Fears associ.9  Hypoactive Sexual Desire Disorder 117 recurrence. More often than self-schema affects how the woman faces cancer not. A quick assessment of dysfunction. ally lead to resentment. Fear and guilt are among the most commonly Relational Factors reported types of negative affect and are fre- quently addressed in the literature. which eventu- the individual perceives and responds to events. fears specific to sexual activities may be decrease in sexual function at 4 and 8 months particularly relevant for understanding sexual postcancer diagnosis [66].

At the time of diagnosis. necrosis. sels in the vagina. greater inhibition of sexual desire. For 50% of when Joan was diagnosed with leukemia. the Radiation Therapy marriage was suffering from polarization around sexual frequency. . David’s can disturb normal motivation (i.H.. This found out that David had an affair. During the later phases of treatment. Since Joan research hypothesized that the increase in sexual was already well practiced at “keeping David dysfunction following radiotherapy is partially happy. when women were tested posttreatment. vagina lead to lack of lubrication and problem- The cancer diagnosis made him afraid Joan atic and painful intercourse. cancer played a positive role when David. His pressure for sex also hid a needy. not always found an association between sexual desire and radiotherapy-induced changes in the vagina. desire) for doctor suggested they talk with a mental health sexual activities. Thus. which then reduces would die leaving him alone in the world. 72]. with higher sexual dysfunction than levels found a common issue in men who have compulsive in healthy controls. Joan also increases after radiotherapy [73. and vaginal adhesion or agglutination. vaginal shortening. It was then Moreover. This posttreatment shift in desire suggests Not only can cancer directly affect sexual desire. 74]. nau.118 A. agreed to elastic vaginal tissue is substituted by fibrous tis- counseling. and vomiting. and sexual dysfunction sexual behaviors [70]. A qualitative study sug- therapy in the treatment of gynecological cancer gested that during treatment patients are mostly are the two most commonly documented inter. At this time. he needed the connection to further engage in sexual activities. Rellini et al. shock of receiving a life-threatening diagnosis than they are about their sexual functioning. 76]. studies that tested desire 1 year post- Effect of Cancer Treatment on HSDD treatment did report a reduction in desire [76. sue present in 78–96% of women receiving dependent man with well-hidden poor self. These somatic symptoms can their sexual function [78]. strongly inhibit sexual desire. quality of Chemotherapy life becomes more important and survival is less of a pressing concern and it follows that women Chemotherapy is accompanied by fatigue. where the ened by the loss of Joan to cancer. However. For example. that the changes caused by radiotherapy may be but as mentioned above the interventions utilized delayed and therefore patients may benefit from to treat the cancer are likely to have adverse consultation for sexual functioning after the ter- effects as well. thus reducing the production of testoster- paring for the sexual side effects that they were one [30]. Chemotherapy and radiation mination of treatment. These changes in the esteem who wanted sex to prove he was loved. physiological changes associated with treatment During the diagnostic stage of the cancer. radiation artificially induces meno- that David and Joan started discussing and pre. In sexual pleasure and therefore the incentive to spite of his affair. Severe sexual desire incom. even Joan and the wealth and prestige she represented. wealthy and well-connected family. David had pressured Joan for sexual inter- course every day.e. During those years. professional on the medical team. radiotherapy [75. focused on their condition and dealing with the ventions that impair sexual desire function. It is important to note that studies have likely to encounter during treatment. threat. 77].” she was determined not to risk a divorce explained by stenotic changes to the blood ves- by denying his sexual “needs.” In this instance. the sexual dysfunctions experienced had been married to David for 10 years. report a greater interest in information regarding sea. Radiation for gynecological cancer is associated patibility is associated with pair-bond dysfunction. pause. she women. She was during the active phase of treatment persist even a high power attorney and came from a very after treatment [71.

desire selected for these studies (more or less went breast conservation therapy [80. it is not clear ment seem to indicate that body image is less whether breast reconstruction can help a woman salient for the sexual function of cancer survi- to increase her levels of desire since there is a vors and that treatments that affect the produc- lack of controlled studies. more studies are needed to and therefore we cannot assume that all women explore potential vulnerabilities that may be spe- would show a similar improvement in their sex. prevention [59. type of cancer for women. more when the tamoxifen treatment was discon- vation with radiotherapy. For a study of breast cancer conser. breast cancer survivors (c. psychological. in a trial for chemo- Breast conservation has been found to be consis. Initially it was believed that one of sexual desire. but results are mixed for its effects on groups. a sample of 86 patients tinued as compared to women who continued a was recruited from an Italian general hospital. little is known on the breast reconstructions usually do not participate psychological vulnerabilities of individuals with in these studies. Oophorectomy tive effect on sexual desire [79]. which is the most common antiestrogen uti. and pendently from the effects of menopause. In addition to breast cancer. therapy compared to mastectomy. These studies did not find a tently better for body image following a cancer significant difference in sexual desire between diagnosis. A paucity of data exists on the sexual side effects of tamox. It is feasible that only women breast cancer. the interpretation of this item is highly breast conservation have reported fewer prob. the lized for menopausal women with breast cancer. not easy and thus. ual function after breast reconstruction. As due to the effect of mastectomy on body image. indicated in our review of the definition of sexual Recent studies have identified menopausal symp.9  Hypoactive Sexual Desire Disorder 119 Breast Conservation Two studies compared women currently taking tamoxefin to healthy women.. the studies on breast cancer treat- image satisfaction among them. Another limitation of tion of steroids may have a stronger impact on the available data is that women not interested in sexual desire. Among breast cancer survivors. than once per month) may cause a ceiling effect However. In these studies. sure of sexual desire and comparing sexual func- efit gained from a less severe loss in body image tion in women taking low vs. after breast removal. was desired sex more or less than once per month. at this point. 81]. Separating the effects Forty-three percent reported they experienced a of tamoxifen from the effects of menopause is decrease in desire that they attributed to the treat. this information is not meaningful if not toms as a much stronger risk factor for HSDD in accompanied by subjective measures of distress. we should inter- ment and 41% reported a decrease in sexual pret these results carefully. Given that sexual dysfunction can who experience greater body dysmorphia after be affected by biological. Two studies Given that there is no set frequency of sexual utilizing random assignment to mastectomy vs. and the mastectomy choose breast reconstruction relational factors. low tamoxifen dose [83]. The arbitrary frequency of sexual lems in sexual desire among women who under. thoughts. cific to women going through breast cancer.f. antiestro- genic medication could potentially have a nega. 81). six studies did not find greater sexual since many women with low sexual desire are desire in women receiving breast conservation likely to desire sex more than once per month. but they utilized a very crude measure of sexual desire. since we cannot desire attributed to the disease [59]. surgical removal of ovaries. high levels of may be overshadowed by the fear that the cancer tamoxifen found that sexual desire increased may return. although some evidence points to greater body Overall. Some exactly identify the effects of tamoxifen inde- women opt for breast reconstruction. desire. Interestingly. oophorectomy. the researchers the major reasons for women to experience a asked participants to indicate whether they loss in sexual desire. which is a prevalent ifen. problematic. is the procedure that . A third study utilizing a more sophisticated mea- Researchers have hypothesized that the ben. 82].

thus a greater likelihood for damage to the vagi. These are multidisciplinary programs which cants which can mitigate painful vaginal issues. In conclusion. It is important to note that the literature consistently points to menopausal symptoms in response to the surgical removal of the ovaries as causing greater HSDD symptoms than natural Conclusions menopause [84. although at a much reduced rate. and therefore it is difficult to identify lated by biological. lems in women with cancer. gram at the University of Vermont Medical cen- mation about pelvic physical therapy and lubri. be the best approach for an oncologist. the production of testosterone continues. This difference has been attributable to the fact that. ter. Oophorectomy may affect sexual desire we are seeing emergence of the inclusion of sex through the reduction in vaginal lubrication and specialists on treatment teams. and tive sexual desire. and particularly hypoac- function. are complex phenomena regu- pain [84]. for this reason. and relational whether the low desire is exclusively the product aspects of the woman’s life and. since 2008. which cause the already low levels of testos. is most commonly identified with a decrease in any improvement in their postoperative sexual sexual desire. have been found to affect all aspects of sexual Sexual dysfunctions. including sexual arousal. While menopause. while surgical Nevertheless. erating new knowledge about sexuality and terone to bind and not be physiologically active. pause. Lately. for Women and Girls with Cancer. ing that point at essential impairments caused by tion of androgen production. a psychologist and/or clinical sexologist. a reason to be avoidant of gram supported by the Department of Obstetrics sexual activities and can provide a lessening of /Gynecology. This is a pro- course is. we can clearly see patterns emerg- menopause causes a dramatic and definite cessa. Therefore. painful inter. it is essential that pre.120 A. treatment of sexual problems in the context of therefore reducing the amount of testosterone cancer treatment and survivorship. Rellini et al.H. However. As we noted above. often with sexual desire. the literature on HSDD in women pause. the changes in the sexual cycle tion become more relevant for women after a caused by oophorectomy are quite pervasive and year of treatment. For the oncol- available to bind with receptor sites involved ogist who has limited time and resources. orgasm. During surgical the side effects of cancer treatments. of course. 85]. during natural meno. of the changes that affected the entire cycle or if the referral to a specialist in sexual medicine may there is a direct effect on desire per se. patients and their partners be advised professionals are also part of the oncological pro- about this outcome and be provided with infor. therapy. a gynecolo- Estrogen administered to women who have gist. in a perspective just introducing the topic about sexual desire and study on estrogen replacement therapy [87]. Section of Gynecology Oncology sexual desire. Mental health emptively. to all function after receiving estrogen replacement intents and purposes. The focus is on gen- els. . the University of Chicago has had a nal epithelium during intercourse which leads to Program for Integrative Sexual Medicine Clinic sexual pain. providing a referral or titles of books (see individuals who underwent salpingo-oophorec. psychological. sexual dysfunc- [86]). androgen levels drop to less than addressing sexual dysfunction in the early acute 50% of the normal production of testosterone in phase of a cancer diagnosis may be relevant only naturally menopausal women (for a review. Indeed. and the Cancer Research Center. Removal of the ovaries. include an advance-practice nurse. induces surgical meno. with a history of cancer is in its infancy. For example. see for a limited number of women. received oophorectomy can also have a negative and a pelvic physical therapist with expertise in effect on desire because estrogen increases levels addressing pelvic floor issues and sexual prob- of sex hormone-binding globuline (SHBG) lev. Appendix) can help the patients and their part- tomy or abdominal hysterectomy did not show ners gaining a perspective on their sexual health.

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Joanne that she had stopped initiating sexual is suffering from female sexual arousal disorder ­activity with her husband. indi- T. and often experienced accompanying pain. Joanne was rarely experiencing lowing cancer treatment. Kukkonen (*) viduals with chronic illnesses like cancer often Department of Family Relations and Applied Nutrition. but Joanne reported that these led to only mild improvement. and found herself feel- Case Example 1 ing preoccupied during sexual activity Joanne. Kukkonen and Sabina Sarin Keywords  Arousal • hormones • androgens • testosterone • estrogen increasingly self conscious about her body due to the physical changes she had noticed since her surgery. age 57. expressed interest in acquiring a prescrip- cantly worsened. with fears that her husband no longer first began experiencing difficulties with found her sexually attractive. sexual arousal a few months after being Joanne noted that she had been unable to diagnosed with cervical cancer. and admitted this chapter is that. 125 DOI 10. Canada tory  and consequently. and was only (FSAD). and ultimately fell into a Americans with a history of cancer [1] and. 50 Stone Road East. By the time that she an increasing number of survivors.1007/978-1-60761-916-1_10. tion for Viagra to help ameliorate her ing surgery. she was rarely able to become difficulties. University of Guelph.3 million during this time. depression and fatigue. (eds. She recalled that follow. Cancer and Sexual Health. Current Clinical Urology. like moderate depression.Chapter 10 Disorders of Female Sexual Arousal Tuuli M. Of particular interest to feelings of ­sexual interest. © Springer Science+Business Media.). Joanne appeared to undergoing a complete hysterectomy.P. In addition. lubricated during attempts at sexual activ- ity. she is strug- presented for treatment (1-year post gling with adjustments to her quality of life fol- ­surgery). may feel uncomfortable J.M. She was reach orgasm during any sexual activity treated with a round of chemotherapy prior over the past 3 months. Guelph. LLC 2011 . such as altered body image. an impairment in a woman’s ability to become She also confessed that she had become physiologically aroused (genital lubrication and swelling) [2]. which has been traditionally defined as occasionally responsive to his initiations. Mulhall et al. highly distressed about these changes and after which her arousal difficulties signifi. among other things. Joanne and her husband began using Disorders of Female Sexual Arousal topical lubricants. In addition. She also reported feeling chronically fatigued Joanne is one of approximately 11. have the added stressor of their illness trajec- ON N1G 2W1. Her case illustrates the often ­complex interaction between sexual arousal problems and other issues. and 6 years ­postmenopause.

In addition. distinction between these constructs.M. As whether it is possible to find pure or primary mentioned earlier. which researchers are now ­suggesting The past three decades have witnessed signifi. 10. Kukkonen and S. describes sequential stages of desire. This multi-faceted circular model of sexual response is based a grow- ing literature that demonstrates the shortcomings Definitions and Problems of a purely physiological linear model [8–14]. 501). FSAD is defined in the cases of FSAD (without other coexisting sexual ­DSM-IV-TR [2] in physiological terms as an dysfunction) [17. relatively little research has addressed this Arousal Disorder. 76% were sity and duration” (p. that even for patients with advanced that “occasional problems with sexual arousal cancer. particularly in female noted that a diagnosis of FSAD should not be cancer patients.” (p.1 tinct diagnostic entity [19]. “more important” things. Sarin addressing quality of life issues such as sexuality for diagnostic criteria and their limitations). non-universal sequence of sexual responses phases [7] (refer to Fig. report survey that do not make the distinction plateau.1. particularly between disorders of arousal and desire. may be one and the same [15. arousal. and the highly overlapping and population. 18]. there cant challenges to the legitimacy of diagnostic is currently no empirical evidence to support the classifications of FSAD. Fig. ­quality of life is as important or more that are not persistent or recurrent or that are not important than the length of life [3]. conceptualization of FSAD derives from the tra- the data that is available on sexual arousal is ditional linear human sexual response model that often based on one or two ­questions in a self. A recent review of the literature made if the arousal problems are due to “sexual found that of 257 articles examining self-reported stimulation that is not adequate in focus. whereas only 15% examined women with breast or gyneco- logical cancers (the remaining 9% examined functioning in other types of cancers) [4]. orgasm and resolution [5. models have been put forward that take into con- lation. however.126 T. These limitations.1). In due to the belief that they should be focusing on addition to the criteria presented in Table 10. this model making it difficult to truly understand the breadth has been subject to much criticism and alternate of female sexual arousal problems in this popu. 501). At present. over recent years. but also accepting sexual activity. Furthermore. However. leading some to question impairment in the genital lubrication-swelling whether FSAD should even be considered a dis- response of sexual excitement (refer to Table 10. aimed at men with prostate cancer. The high degree of overlap amongst the dif- ferent phases of sexual response in women has Diagnostic Criteria for Female resulted in a high comorbidity in sexual dysfunc- Sexual Arousal Disorder tions. inten- sexual functioning in cancer patients.2). 16]. . the current breast and gynecological cancers. it is unclear as  a diagnostic marker of sexual arousal. contextual factors in appear in the literature on FSAD in the general sexual response. 6] (refer to between mental and physiological sexual arousal. the DSM-IV-TR text also includes the qualifier however. Indeed. substan. sideration multiple motivations for initiating and cific to studies on women with cancer. While sex. 10. it is issue in cancer patients. The Models of Sexual Response limited data evaluating sexual functioning in women with cancer is ­heavily weighted towards As with the other sexual disorders. and women tial debate has focused on the relative importance themselves report extreme difficulty differentiat- of subjective versus physiological excitement ing these responses [16]. are not spe. In particular. accompanied by marked distress or interpersonal ual health is an integral component of quality of difficulty are not considered to be Female Sexual life. Research indicates.

(b) Context – generalized Type vs.g. or maintain The ambiguity of the requirement that symptoms be until completion of the sexual activity. of genital response alone is insufficient to diag- nostic marker of an arousal disorder (Criterion A) nose arousal problems in women. a medication) or a general medical condition Specifiers: (a) onset – lifelong type vs. addition. it is clear that the criterion jective feelings of excitement. dysfunction) and is not due exclusively to the causes are multifactorial or difficult to determine physiological effects of a substance (e. While the reasons for desynchrony have (i. women on genital arousal cues in their apprais- ible and context-based models has served to als of subjective arousal. acquired type. research indicates that even women Adapted from Kaplan [5] without self-reported arousal difficulties com- monly experience desynchrony (low or non- existent correlations) between subjective and Problems with the DSM genital measures of sexual arousal [22]. as the sole diag. and of limited utility has been demonstrated to be overly narrow and thus inadequate (refer to Graham [20] for more details). the formulation of more flex. and swelling of the external The criterion of genital arousal impairment as the sole genitalia diagnostic marker of FSAD is insufficient and not supported by research The disturbance causes marked distress or Whether distress is considered as a diagnostic requirement ­interpersonal difficulty dramatically affects prevalence estimates of FSAD. and (c) Etiology – due to psychological epidemiological researchSpecification of etiological factors vs. Specifically. rates are inflated when distress levels are not assessed The sexual dysfunction is not better accounted for by The feasibility and utility of determining the exclusive another Axis I disorder (except another sexual cause of a sexual problem is not high.. In particular.10  Disorders of Female Sexual Arousal 127 Table 10. 23]. situational these distinctions have rarely been made in type. studies employing vaginal photoplethysmography (VPP) [21] an indirect measure of genital arousal – have rarely found significant differences between medically healthy women diagnosed with sexual arousal disorder and healthy control women [22. lubrication/swelling).e. the insufficiently arous- highlight some fundamental limitations in our ing nature of the erotic stimulus used in the current diagnostic conceptualization of FSAD laboratory context. the tools used to measure sexual arousal in women requirement of an impaired genital response [22].1  DSM-IV-TR diagnostic criteria for FSAD and their limitations Diagnostic criteria Limitation Persistent or recurrent inability to attain. In most cases. an “persistent and recurrent” places excessive reliance on adequate lubrication-swelling response of sexual clinician judgment to decide what these terms mean. contrary to women’s ­clinical and epidemiological reports of insuffi- cient genital arousal. Although clinically useful to specify onset and context. and the limitations of the (presented in Table  10. 10.. .1  Masters and Johnson model of sexual response. including women’s lesser While consensus has not yet been reached about awareness of the genital changes accompanying how to best capture the complexity of female their arousal. a drug of abuse. due to combined factors factors is often impossible. The arousal response consists of Decisions may negatively affect clinical and epidemio- vasocongestion in the pelvis.1). to the neglect of sub. the lesser importance placed by sexual experiences. In Fig. conceptualization of FSAD Numerous theories have been offered to account for this phenomenon. vaginal lubrication logical research and expansion. excitement. not been established.

. illness/medication) scale epidemiological surveys with nationally a  Recommendations for duration and severity of symptom representative and cross-cultural samples. duration. Kukkonen and S.g.128 T. Medical factors (e. Sarin Fig... three indicators occurring for at least prevalence of arousal difficulties in women 6 months) currently rest on sparse empirical evidence.. the occurrence (e. of at least 6 months Given the above limitations. and the lack of evi. .. relationship discord.2  Basson’s circular model of female sexual response.M. poor communication. discrepancies in desire for Epidemiology sexual activity) Individual vulnerability factors (e. history of abuse Lifetime Prevalence of FSAD experiences) Cultural/religious factors (e. poor body image.2 for proposed criteria). No initiation of sexual activity and is not receptive to a partner’s attempts to initiate egory heading of “Sexual Interest/Arousal Absent/reduced sexual excitement/pleasure during Disorder” [20]. it has recently been recommended that Absent/reduced interest in sexual activity the diagnostic categories of sexual desire and Absent/reduced sexual/erotic thoughts or fantasies arousal disorders be collapsed under the new cat. encounters) nosis of this disorder to recognize the heterogene. Absent/reduced genital and/or non-genital physical ity in women’s expressions of low sexual interest/ changes during sexual activity (on at least 75% or more of sexual encounters) arousal. as manifested by at least 3 of the following dence to support the distinction between arousal indicatorsa: and desire.g. Adapted from Basson [142] Proposed Criteria for the DSM-V Table 10. These suggestions have or impairment been incorporated into the symptom criteria that Specifiers: have been proposed for the DSM-V (refer to Lifelong or acquired Table 10. Generalized or situational Partner factors (partner’s sexual problems.g. inhibitions related to prohibitions against sexual activity) Despite the recent publication of several large.g. and to avoid prioritizing one symptom The disturbance causes clinically significant distress presentation over another. 10. In addition.2  Proposed DSM-V criteria for sexual interest/ arousal disorder Lack of sexual interest/arousal. depression or anxiety. partner’s health status) Relationship factors (e.g. it has been advised sexual activity (on at least 75% or more of sexual that a polythetic approach be applied in the diag.

teria (e. type of cancer [30]. In addition. as did sexually active [28]. With respect variety of cancers and found that 36% of the to the latter. and duration of the difficulty (i. or other con- textual variables) (for a review. the lems and/or the recall period specified. with higher rates found in women between frequent comorbidity with other sexual disorders the ages of 50–59.1% (Southern Europe) to 37. In addi- tion. in women undergoing neo-adjuvant chemother- itally aroused). Huyghe sus subjective feelings of excitement/pleasure or and colleagues examined men and women with a other physiological responses) [20].. There is currently no epidemiological informa- odological limitations in assessing arousal diffi. and how arousal difficulties are opera. As compared to medically healthy women. prevalence Finally. With these qualifications in mind. Finally. tress. and 29% prevalence rates of questionable validity. In a recent study. see [20]).g. (e.2% of women had surviving chronic myeloid leukemia indicated short-term difficulties with lubrication.. survey methodology (e. the majority of survey studies have women noted problems with sexual excitement assessed problems exclusively with lubrication. postmenopausal women from follow up [35].g.7% decreased sexual functioning as compared to the had persistent problems (lasting at least 6 months) general population [34].g. and pleasure following cancer diagnosis.9% (East Asia). its 12. rates are Similar to patients in the earlier stages of diag- higher for older women. 16. level of dis. objective evidence) and the challenges in distinguished from subjective appraisals of geni- determining the etiology of arousal problems via tal arousal. the duration of sexual prob. Speer and colleagues . Tierney and colleagues found similar rates evidence of an impaired potential to become gen. as due to a medical condition. and for those with short. with dents indicated serious problems in at least one rates varying as a function of age. inadequate stimulation. nosis and treatment. long-term cancer survivors term difficulties and mild/no distress) [24–27]. ranging from 25 to over 50% depending on the tionalized (e.. with estimates sampled. female oncology population has higher rate of culture and reproductive status of the women difficulties with sexual arousal. At a median a study with women between the ages of 18–44. particularly as vs. and Given that impaired genital responsiveness may 46% of them reported a problem with vaginal not be a valid diagnostic criterion of FSAD in lubrication after cancer diagnosis and treatment medically healthy women (due to the minimal [31].g. than those aged 40–49 [29]. the age..e. a study examining sexual functioning in rates of arousal difficulties have ranged in studies women during the first months following breast from approximately 7–31% (averaging around cancer treatment showed that 28% of respon- 14%) for women between the ages of 16–75.. prevalence rates vary dramatically depending Prevalence of FSAD in Cancer Patients on whether the presence of “distress” or “inter- personal impairment” is evaluated or required for disorder diagnosis. regarding what should be considered and of “frequent” problems ranging from 4. only 3. low desire and orgasmic difficulties).10  Disorders of Female Sexual Arousal 129 remains unclear. as problems with lubrication ver.g. studies defining arousal difficul. follow up period of 8 years. ­discrepancies between self-report tive sexual excitement difficulties. apy for hematologic cancer with 36% reporting ties in these terms have arguably produced problems with arousal and pleasure. area of sexual functioning [33]. tion available on the prevalence rates of subjec- culties (e.. one third of patients it was estimated that while 9. meth. one of the few epidemiological survivors of gynecologic cancer at a 2-year studies with older.1%. In also report difficulties with arousal. noting difficulties with vaginal dryness [32].7 to reflective of “adequate” sexual stimulation). Estimation of prevalence rates 29 different countries found prevalence rates of of FSAD has been complicated by various ­factors “occasional” lubrication difficulties ranging from including the ambiguity of FSAD ­diagnostic cri.

a disorder decreased estrogen is associated with vaginal has frequently been associated with sexual dys- atrophy. and certain pharmacological patient’s life (e. however... undergoing chemotherapy may experience a While decreased lubrication in postmenopausal decrease in libido and increased vaginal dryness women is typically attributed to lowered estro- as a result of her medication. and health medications including antihyperten- sives. but rather. Sarin noted that long-term survivors of breast cancer neurological. had significantly lower scores on the Female arousal difficulties in women (i. results problems will interact with each other to exacer- have been inconsistent. there is some evidence indicating that exhibiting symptoms of depression. In one exceptional cardiovascular disease.. and women indicates that arousal difficulties in this hence. Specifically. as indi- arousal difficulties in women. hormonal. While the past cated by changes in VPA [46]. ovarian.. cancer treatments. they interact ditions (e. the relationship treated for medical or mental health conditions. hypothyroidism. premenopausal difficulties in women remains understudied. lifestyle factors such as tobacco/ Until recently.g. neurogenic or neurological study. cantly higher than medically healthy women who breast. hyperprolactinae- mia. Greenwald et al. In particular.g. This is particularly pausal and postpartum status) have also been true of patients with cancer where comorbid correlated with lowered arousal [42–44]. For example. making aging an even stronger risk factor for arousal difficulties in The relationship between different physiological women. 90% of long term cervical cancer survivors had vulvovaginal atrophy or connective tissue damage. they scored signifi. and the relationship bate arousal disorders. cervical). hysterectomies/ with each other and with other aspects of the oopherectomies)..g. Kukkonen and S. drugs such as antidepressants and antipsychotics.130 T. It is likely that neither the chemother- Aside from medical health conditions.g.e. multiple sclerosis. enjoyable sex lives though questions specific to urinary incontinence and lower urinary tract sexual arousal were not asked [37]. and H2-blockers. conditions such as reproductive cancers (e. anticonvulsants. Many of Correlates of FSAD these factors also have a strong independent association with age. vascular. decreased Sexual Function Index (FSFI) than women in the lubrication) have been associated with medical general population.. Finally. The research currently group are more often associated with inadequate available supports an association between female sexual stimulation than with physiological sexual dysfunction and a number of medical and causes [47]. ­psychiatric arousal disorder. Although certain phases of the men- and psychological factors to sexual arousal prob- strual and reproductive life cycles (e.g. In contrast to decade has witnessed a surge of interest in the research with women struggling with or being pathophysiology of FSAD. ovarian failure.M. a patient between these factors is poorly understood. poorly understood. but she may also be gen levels. pharmacological). found that over impairment.. there had been little examination nicotine use have also been correlated with of the physiological factors underlying sexual impaired genital response in women. however. . between physiological risk factors and arousal research with medically-healthy. estrogen deficiency. have all Physiological Correlates been associated with arousal difficulties in women [40]. diabetes. and congenital adrenal hyperplasia (for reviews see [38–41]). function. meno- lems is often overlapping. but not vaginal dryness [45]. medi- apy nor the depression is entirely responsible for cal and surgical treatments for various health con- the arousal problems. hypertension/ suffered from FSAD [36]. problems. health related factors (e. relationship with her partner treatments have also been associated with arousal and other life stressors) to bring about the sexual difficulties in women.

women who were irradiated known. to having a detrimental effect for women with phy and shortening of the vagina. sexual arousal are not well documented. In addition to the direct sexual side have to deal with the hormonal fluctuations effects. have all been associ. the ing more than 7 years after diagnosis and treat. increased genital pain [53]. infection. reduces the amount lower sexual functioning than those who under- of circulating estrogens and induces menopausal went surgery for the same cancer [56]. decreased lubri. alopecia. Even within the cal toll on the body. For example. hormone therapy has also been significantly better sexual functioning than those associated with vaginal atrophy. radiation therapy. This may increase vaginal dry- ments for cancer-chemotherapy. ness and make intercourse painful. For example. inal tissue and significant changes in the vaginal toms [48]. Further­more. undergoing oopherectomy [37].. with tioning. radiation can also indi- negatively affect sexual arousal [39]. doses and combination therapies. the new tissue is histo- drugs. a woman decreases in sexual arousal and desire. Furthermore. rectly affect sexual arousal due to the pain and els of estrogen have also been suggested to restrict scarring of the skin at the site of radiation (e.10  Disorders of Female Sexual Arousal 131 Physiological Considerations for Cancer effects of chemotherapy. as well as undergoing surgery to remove part of her calf due increases in sexual pain [50]. all of which a woman’s sexual arousal in distinct ways. In contrast to the bleeding and loss of organ function. decreased libido and sexual arousal. a recent study has shown that women engage in sexual activity. decreasing sexual arousability. which in turn. with recovery time and can alter their sense of body reports of decreased sexual functioning continu. nipple and breast pain for breast cancer) as well as vation. vaginal atro. in women with cervical patients having reproductive cancers or hormonal cancer. The While the surgeries for both these women require effects of chemotherapy can be long term. with patients often reporting same type of cancer. however. and typi- While a tumor itself can directly affect sexual cally reverse upon treatment discontinuation. undergoing hysterectomy for cervical cancer had Similarly. hence impairing sexual arousal. Surgical treatments may also differentially In line with this. General side cation. genital vasocongestion through sympathetic inner. logically different and may lead to decreased cific mechanisms by which chemotherapy affects blood flow and impaired genital response [55].g. a significant proportion of impact female sexual arousal depending on the women undergoing chemotherapy report site and type of operation. however. with cancers in the pelvic region are most likely to mones. In addition symptoms such as vaginal dryness. all of which . while re-epithelialization can occur within 6 Due to the number of different chemotherapy months for most patients. fatigue. thereby hormone therapy and surgery. it has to sarcoma may not necessarily experience the been shown that women undergoing chemother. chemotherapy also takes a strong physi. the most common treat. that chemotherapy can initiate for cervical cancer demonstrated significantly ovarian failure. and effects from surgery also include pain. undergoing other forms of treatment [51]. epithelium [54]. the sexual Patients side effects of hormone therapy have been found to last as long as the treatment itself. and pain. all of which gynecological cancers. it is often the treatment of cancer that has experience direct effects related to sexual func- the largest impact on sexual functioning. arousal through the restriction of blood flow to the Due to the local nature of radiotherapy. patients genitalia or disruption to the production of hor. It is Congruent with this. the spe. brachytherapy leads to fibrosis of the vag- imbalances experiencing the most direct symp. different surgeries can affect nausea. For can impair one’s quality of life and desire to example. Specifically. image. ated with increased sexual dysfunction in women. become physiologically sexually aroused [49]. which directly affects a woman’s ability to due to more general side effects such as fatigue. induced by early menopause. woman undergoing a full hysterectomy will also ment [52]. Reduced lev. same dampening in her sexual arousal as a woman apy score worse overall on the FSFI than those undergoing full hysterectomy for cervical cancer.

ically significant levels of depression are consis. cognitive and psychoso- on female arousal disorders specifically. due to daily stressors. reaction. however.g. desire or sexual there are other antidepressants that have been script discrepancies. Sarin may influence the process of sexual arousal. anxiety. Cognitive variables. inadequate sexual the vaginal wall or reproductive organs. though SSRIs have many difficulties in women [26]. Psychological Correlates for FSAD Psychological Considerations for Cancer Although it is well known that psychological fac. . Buproprion) [71. depending on their secondary binding properties. Other niques [27]. is also strongly associated with impaired arousal cally associated with a higher incidence of arousal [36. noted. 32% suffer from moder- low self-esteem. 60]. Kukkonen and S. associated with better sexual side effect profiles incompatibility. 70]. For example. 62]. female patients with either depression or anxiety tently found to predict disorders of arousal as may be more likely to focus on stimuli that is not well as desire [61. Basson model of sexual response (see Fig. depression. The cial factors contribute to sexual arousal disorder research that currently exists suggests that emo. lower education level.g. fatigue. of impairment in sexual responding [70]. dis. poor sexual stimulation. self. correlations do not months after surgery [58. clin. general dissatisfaction/distress. and engaging less sexual self-image and levels of self-consciousness frequently in sexual activity [26]. relationship factors com. Specifically. Some of the strongest advantages for cancer patients (e. being married.” or negative body and anxiety on arousal in cancer patients. on the lated with arousal problems include lower face or neck). research image) have also been found to predict dampened indicates that pharmacological treatment with sexual arousal [29. low side predictors of reported arousal problems in women effect profile.g. It is estimated that any- tional variables such as negative affect or poor where from one third to half of oncology patients mental health status (e. 10. or an (e. Patients tors play a strong role in the etiology of female sexual dysfunction. lack of intimacy/trust. 66]. up are relationship difficulties and partner variables to 96% of women taking SSRIs report some kind [27. a stoma. in women with cancer.. sexual interactions. In addition to the effects of depression consciousness/“spectatoring.g. and ­distraction from erotic increased heart rate) as an unpleasant or negative cues (e.M. 59].2). there is selective serotonin re-uptake inhibitors (SSRIs) evidence that a history of sexual abuse is specifi. 72]. ate to severe fatigue and 18% suffer from tress) are commonly been linked with arousal ­significant anxiety [67–69]. If we examine the difficulties in women [29. Other psychosocial variables corre- surgeries which leave visible scars (e. It should be [58]. with deterioration or tioned variables have been found to be associated decreased sexual functioning found 12 or more with arousal difficulties.. Partner variables have included a part- ficulties are surgeries that require the removal of ner’s sexual dysfunction. experience depression. safe to use with chemotherapy). can significantly affect an individual’s unemployment. or those that require the creation of socioeconomic status. there has been minimal There are numerous ways in which the afore- examination of the influence of these variables mentioned emotional. text [27]..g. disordered eating. otherwise inappropriate/non-optimal sexual con- More obvious contributors to sexual arousal dif. While monly associated with arousal difficulties include different SSRIs may yield differential effects relational conflict.. that while all of the aforemen- geries are long-lasting. Finally. imply causality. the sexual side effects of some sur.. In particular. longer relationship duration. 63–65].132 T. Additionally.g. such conducive to sexual arousal or may mislabel as negative sexual attitudes/expectancies about physiological indicators of sexual arousal (e.. and the mechanisms through which these variables are associated with arousal problems is still poorly understood. such as knowledge and/or poor sexual stimulation tech- hysterectomy or radical cystectomy [57].

. hematopoietics).. Buproprion. more negative attitudes woman’s sexual self-schema (how she views towards sexuality and were limited in initiating herself as a sexual being) can also affect sexual intimate relationships as compared to the gen- arousal. 82]. One additional psychosocial consideration oids. in examining the existence of sexual macy were an important part of their quality of arousal problems in cancer patients. 84]. younger women who have menopause induced ness to engage in sexual activity and may also due to treatment are at greater risk for sexual decrease feelings of sexual arousal [35]. and counseling regarding sexuality. Cancer patients with positive sexual eral population. highlighting the importance of self-schema have been found to have signifi. unmarried patients [81].g. Furthermore. a lower rates of marriage. 30% of cervical can. appearance can significantly affect ones willing. In addition. the comorbidity of fatigue with depression. Research has shown that married patients seems to persist well after treatment has ended.. nosis of cancer and its treatment can also have a In non-cancer populations of chronic fatigue. Body dysfunctions and also are significantly more dis- image can also interact with relationship func. intimacy Negative feelings towards ones own body/ and fertility options [83. corticoster. cope better with their cancer diagnosis than According to Vistad et al. SSRIs and ities. it is conceivable that the gen. cantly more frequent sexual activity. others have not been shown to have they were purposely avoiding intimacy [32]. Similarly. more than half of women indicated that Modafinil). with whose physical appearance has been altered by younger patients having great need for guidance surgery or by the addition of a stoma [77. found that relationship distress accounted for a anxiety and pain. and higher sexual satisfaction than life may not necessarily engage in sexual inter- those with negative sexual self-schemas [80]. physical activity. however. addressing these issues in a clinical setting [86]. As difficulties with sexual arousal in female cancer chronic fatigue significantly dampens levels of patients [33. Fobair et  al. often accompanied by adjustments to body Arousal difficulties will likely affect patients image in cancer patients. However. found that Research indicates that patients with chronic women who felt that their partners did not under- fatigue have significantly lower quality of life. Additionally. given than those who did not. 36]. While some pharmacological treatments patients and partners do not necessarily report for cancer related fatigue can increase the inci. course. 78]. for female sexual dysfunction in cancer patients Impairments in mood and energy levels are is the phase of life cycle in which it occurs. changes in their ability to engage in sexual activ- dence of sexual dysfunction (e.10  Disorders of Female Sexual Arousal 133 In addition to depression and anxiety. tressed by changes to their appearance than older tioning such that women report feeling more patients who have already gone through meno- attractive and having better sexual encounters if pause at diagnosis [85]. marital sat- cer survivors continued to suffer from chronic isfaction in cancer patients has been found to be fatigue 5 or more years following radiotherapy positively related to better sexual experiences as compared to 10% of general population [73]. the diag- detrimental effect on their sexual activity [75]. negative impact on intimate relationships [37]. studies have found that while [76]. stand their feelings were significantly more increased anxiety and depression and more likely to experience sexual arousal problems physical complaints [73. fatigue ignore the relational context in which the disorder is a common side effect of cancer therapies that occurs. it is difficult to ascertain the significant proportion of the variance found in direct impact of fatigue on sexual arousal. an adverse effect (e. while patients at the end of their ual response.g. particularly for those differently depending on their stage of life. one cannot life [87]. research indicates that sexuality and inti- Finally. no direct link has been established For example.. [79. A review of the litera- they perceive that scars from cancer surgery do ture shows that childhood cancer survivors have not bother their partners [79]. In addition. 74]. Moreover. While relationship functioning can influence eral lack of energy felt by patients will have a the experience of sexual dysfunction. better sex. Speer et  al.

[89]. has taken guilt and embarrassment because they want to over most of the household tasks in an engage in sexual activity despite mortality and attempt to reduce Sara’s stress. whereby a woman’s personal history. Furthermore. to the point where she is having diffi. physiological and psychologi- cal health. Sara has gone on patients may not present with a sexual arousal sick leave from her job as a flight attendant disorder per se. they may experience significant and her partner of 8 years. while both case from Claire and is avoiding all forms of examples raise distinct sexual issues. It is important that the clinician rec- nosed with stage 2 non-small cell lung can. Kukkonen and S. such as cer. the immediate focus of treatment should awaiting surgery and has been referred to be dealing with the sleep and mood disorder. 93]. and it is the clinician’s job the  course of the assessment. therefore. It is important. research has also found that female partners of cancer patients are at greater risk for depression. patients are intimacy with her after a recent sexual often hesitant to discuss sexuality within the encounter where she had difficulty becom. Finally. in a population of men with prostate primary source of disagreement between cancer. ognize that under some circumstances. At the time of assessment.M. priate to explore the source of the couple’s dis- culty sleeping at night and cannot function agreement. arousal. but can also be agreed to palliative treatment for metastatic found in partners of patients with cancer. to normalize their experiences and present a non- cates that she has felt herself pulling away judgmental attitude. she is Sara’s. Her husband of 40 years. partners reported significantly greater the couple revolves around Maude’s wish sexual dissatisfaction than non-clinical samples for sexual relations with her husband. as well as her relationship functioning Assessment and environmental factors are considered in the case formulation [92. Within the context of cancer. Sarin FSAD in Partners of Patients Case Example 3 It is important to note that FSAD does not only Maude is 65 years old and has recently occur in the oncology patient. Sara indi. satisfaction [90]. arousal difficulties will present them- selves amidst a myriad of physical and psycho- Case Example 2 logical difficulties as noted in the cases of Sara Sara is a 43-year-old woman recently diag. psychology due to increasing levels of anx. sexual arousal difficulties in women involves a biopsychosocial approach. Fisher et  al. it is discovered that a Similarly. and Maude. In addition to the effects on sexual dysfunction. which is a strong predictor of The standard recommendation for assessing levels of sexual satisfaction [89. In a breast cancer. 91]. while some cancer properly during the day. Claire. partners of men with prostate Maude is embarrassed by her sexual desire cancer indicated high levels of sexual dysfunc- and George emphasizes she should be tion that were negatively associated with marital focusing on more important things. such as Maude’s. doctors would be dismissive or embarrassed by the topic [94]. context of cancer because they fear that their ing lubricated. decreases in desire. whereas in others. found that George. During chronic health issues. orgasm and sexual During an assessment with the ­palliative satisfaction following the diagnosis of ED [88]. non-cancer sample. case psychologist. is having a difficult time accepting women whose male partners had erectile Maude’s prognosis and the couple find ­dysfunction (ED) were more likely to report themselves arguing over a number of issues. Additionally.134 T. it is appro- iety. as a .

Rather. value when it is the cause of the arousal diffi- and may include a few items that are pertinent to culty that is in question. such physical impair- much information as possible (see Table  10. caution should be exercised in inter- the woman’s difficulties.g. psychological and social factors clinicians may also employ one or more of a assessed to influence the women’s sexual experi- number of self-report measures of sexual func. and four pertaining to gen- Clinical Assessment of FSAD eral subjective arousal). Moreover. in order to gather as sexual dysfunction. adjuncts [95]. with broaching the subject of sexuality with The two measures that include a more detailed patients and that one demonstrate a willingness assessment of arousal difficulties are the FSFI to openly discuss the topic.10  Disorders of Female Sexual Arousal 135 health care provider. Finally. self.3) ments represent one piece of information to be [92. considered within the context of all the other As an adjunct to the clinical interview. While these measures provide a more comprehensive assessment of Despite evidence of the desynchrony between arousal difficulties in women. both of which include eight ques- tions devoted to arousal (four regarding genital arousal-lubrication. clinicians may also choose to administer self- ance on the clinician’s judgment of the patient’s report measures of sexual satisfaction and rela- self-reported difficulties. ence. In the and to maximize the potential for obtaining case of non-medically healthy women. these exams of this.. In the assessment of sexual dysfunction [96]. rather than dysfunction-specific. arousal and her actual genital response. estrogen have advocated a biopsychosocial assessment of deficiency). as part of their diagnostic assessment of arousal ized or psychometrically validated for the difficulties (see Table  10. the majority when abnormalities are identified (e. Finally. however. [99] and the Sexual Function Questionnaire (SFQ) [100].g. in which diag. tionship adjustment.3 for examples). in addition to comprehensive clinical interview. it is important to note that in all of tioning [96–100] (see Table 10. with the caveat that the preting the results: the presence of an abnormal- woman and her partner be interviewed both ity should not implicate it as the cause of the together and separately. in view of the lack of arousal difficulties has unfortunately relied concordance between a woman’s reported almost exclusively on a woman’s self-report. difficulties. cal exam is highly recommended. FSAD). In view case of medically healthy women. clinicians and researchers have recently typically do not identify a cause of the arousal proposed numerous guidelines and recommen. to date. 93]. a physi- diagnostically useful information [92. that one be comfortable the sexual difficulty in question (e. they may prove to be reas- dations to better structure the interview process suring for the woman and her clinician. Last. however even As part of these recommendations. in order to augment their report measures of female sexual functioning comprehensive diagnostic assessment of arousal and physical exams are also used as diagnostic difficulties [95].. sexual functioning. clinical cutoffs for the domain score do not cur- the assessment and diagnosis of female sexual rently exist.3 for details). On occasion. in many cases a clinician view to making diagnoses. the above cases. some nosis of sexual dysfunction is achieved via reli. measures assessing sexual functioning. an examination of the genitalia Most of these are global measures of sexual in a nonaroused state can only be of limited functioning. in addition to self-report measures of In spite of the centrality of the clinical inter. the reli- This typically occurs in the context of the clinic ability of the information provided by these (by treatment-seekers) and takes the form of a measures is questionable. . 95]. neither has been women’s reports of genital arousal difficulties validated as a diagnostic tool for FSAD and and their objective genital response. there is currently no may also recommend a physical and pelvic exam widely used interview that has been standard. many biological. 93.

Sarin Table 10. context of problem Provides information on the presenting ●● Motivation for seeking treatment problem and possible contributing and ●● Examination of biological factors maintaining factors ○○ Health ○○ Lifestyle ○○ Hormone levels ○○ Medical conditions ○○ Surgeries ○○ Physical trauma ○○ Medication use ●● Individual psychological factors ○○ Mental health ○○ Emotional health ○○ Thoughts and emotions during sex ○○ Past sexual experiences ○○ Trauma history ●● Social and relational factors ○○ Ethnocultural and religious attitudes ○○ Partner communication ○○ Physical attraction ○○ Sexual compatibility ○○ Trust within the relationship ○○ Partner sexual health. extent. mental health.3  Multidimensional assessment of female sexual arousal disorders Clinical interview ●● Nature. Kukkonen and S.M.136 T. physical health ○○ Partner reaction to problem Self report measures ●● Female Sexual Function Index (FSFI) Provides quantitative information on ●● Sexual Functioning Questionnaire (SFQ) extent of sexual problem ●● Brief Index of Sexual Functioning for Women (BISF-W) ●● McCoy Female Sexuality Questionnaire (MFSQ) ●● Derogatis Interview for Sexual Functioning (DISF) Physical/pelvic assessment ●● Non-genital features Provides information on physical features ○○ Estrogen deficiency that may be contributing or exacerbating ○○ Connective tissue disease the problem ○○ Systemic disease ○○ Disabilities ○○ Disfigurement ●● External genitalia ○○ Sparsity of pubic hair ○○ Vulval skin disorders ○○ Fissures in interlabial folds ○○ Labial abnormalities ●● Introitus features ○○ Signs of vulvar disease ○○ Pallor ○○ Friability or loss of elasticity/moisture from vulvar atrophy ●● Internal features ○○ Pelvic muscle tone ○○ Hypertonicity of muscles ●● Full bimanual features ○○ Fixed retroversion of uterus ○○ Uterine tenderness Psychophysiological assessment ●● Thermography Provides a measurement of genital ●● Labial thermistor functioning in an aroused state ●● Laser Doppler imaging ●● Clitoral ultrasonography ●● Vaginal photoplethysmography ●● Pelvic MRI .

but the medical practitioner’s physical and genital rather. remains inconclusive.10  Disorders of Female Sexual Arousal 137 Hence. response. one a multidimensional approach be employed in the must keep a broad definition of sexuality and under- assessment of female sexual arousal difficulties. but also the researcher’s sual touch back into their relationship. and the woman’s self-report measures of with nudity following surgery. Several off-label applications of arousal difficulties. nor do they impact vaso- rate components that address the physiological. or genital arousal sensations. which will be central to developing appro. Within the context of cancer. The majority of these remain in their investigative infancy (particularly in terms of their diagnostic validity). Both these psychophysiological assessment measures. vasoactive agents. such as thermography [102. stand that the traditional goal of directly increasing which incorporates not only the data from a clini. either/ psychological. examining the drugs for FSAD have recently been considered. However. the patient may wish to increase comfort exams. acting agents and hormonal therapies. all of which serve as controlled trials to support the use of any partic. Thus. and relational factors identified in both of which may be impaired in women with the history to be contributing to the patient’s reported sexual arousal difficulties [104]. and can thus indirectly increase a to measure female sexual arousal (see Table 10. the treatment for women reporting Treatment Overview of FSAD difficulties with genital arousal has involved the administration of topical lubricants. neurotransmitter- that practitioners incorporate these tools as a rou. patient’s ability to feel sexually aroused. as There are currently no medications that have they overcome many of the limitations of previ. and incorpo. it is recommended that implementing psychological interventions. in light of this. evidence regarding the effectiveness of these tion about what likely occurs physiologically for agents in the treatment of arousal difficulties the woman when she is in a “real-life” sexual situ. Topical Lubricants Most often. and as such. tine component of the multidisciplinary package used to assess female sexual arousal difficulties. some Biological Interventions of these instruments. . cosmetic remedies for an insufficient lubrication ular intervention for FSAD. these drugs fall ation. however. Overall. Specifically. it is recommended lubricants. hold great promise as diagnostic tools. There is currently limited data available from vitamin E.3). be feasible or important to the cancer patient. While sexual difficulties. Administration (FDA) for the targeted treatment tive picture of the nature of a woman’s reported of FSAD. creams. have not yet been put to full clinical use (for review see [101]). congestion. it is gen. or to integrate sen- sexual functioning. sexual arousal to aid in sexual intercourse may not cian’s comprehensive history taking interview. as they have no long-term follow a biopsychosocial approach. The utility of these lubricating aids is erally recommended that treatment of FSAD limited. in traindicated with treatment of cancer in women. Additionally. effects on lubrication. or mineral oils. been approved by the Food and Drug ously used instruments and provide a more objec. within four general categories: topical creams/ priate treatment plans. There goals can lead to increased comfort with oneself are currently a host of psychophysiological tools and one’s partner. and the erotic stimulus will provide invaluable informa. 103]. they offer a rela- the possible interaction of biological interventions tively benign treatment option that is not con- with the treatment of cancer itself. genital arousal response during exposure to an but controlled studies are few in number. However. lubricants do not have an impact on improving treatment of FSAD must take into consideration the underlying cause of FSAD.

and efficacy of phosphodiesterase 5 inhibitors sexual satisfaction. The results from these studies have. In addi. while pausal women. those with objectively reduced genital vasoconges. Results from the menopausal.. . such as sildenafil. ephedrine. as well as buproprion (a dop- domized controlled studies found that while the amine reuptake inhibitor and norepinephrine pharmacological agents of yohimbine. Central Nervous System Acting Agents tion). perceived nitric oxide and adrenergic systems are impor- genital arousal. and so direct compari- vasodilators in pre. in women with and without (PDE5s) in treating erectile difficulties in men. 110]. owing in part to differences between these inhibitors can improve genital vasocongestion in studies in sample composition and measure- patients on SSRIs [108]. drugs such as apomorphine or levadopa (dop- tolamine) [104. with reported arousal difficulties. amine agonists). l-arginine agonist).138 T. an antihypertensive medi- studies in this area have primarily concentrated cation that acts as a selective adrenergic agonist on the utility of sildenafil citrate (Viagra) – a (thus blocking sympathetic nervous system PDE5 inhibitor that functions to increase genital activity). arousal-enhancing pharmacological agents has In addition to research with the PDE5s. been mixed [72. 114. 115]. l-arginine. there focused on the use of drugs that amplify genital has also been some investigation into the vasocongestion. Kukkonen and S. and orgasmic potential for tant in facilitating sexual arousal in women. it may be that ment tools. genital arousal levels were not there have been parallel attempts to test these measured in this study. found that sildenafil did evidence from these studies suggests that both lead to increases in subjective arousal. functioning of women with low desire [72].M. Two of these ran. phentolamine (an alpha adrenergic antagonist congestion. FSAD. tive measures of arousal [113]. it has no impact on subjective reports and vasodilator) have been found to produce of arousal.g. arousal. agents targeting these systems remain inconclu- tion. phine and buproprion) on the reported sexual tive ratings of arousal [104. In contrast. has been found to dampen both physi- vasocongestion through nitric oxide mediated ological and subjective levels of arousal in pre- smooth muscle relaxation.. there is some evidence that the use of PDE5 sive. Controlled studies on clonidine. One mild increases in both physiological and subjec- exceptional study with estrogenised postmeno. Sarin Vasoactive Agents Ferguson and colleagues [109] found that Zestra (a botanical massage oil) led to increases in In view of the body of evidence supporting the subjective levels of desire.e.and post-menopausal while some researchers have found a facilitating women with and without sexual arousal dis. there have also been recent ­effectiveness of other vasodilating drugs that attempts to test the effects of central nervous act to increase smooth muscle relaxation via system (CNS)-acting agents (which act as neu- nitric oxide-mediated processes (e. are useful for a spe- cific subgroup of women with FSAD (i.g. sexually functional women [112]. effect of dopaminergic agents (i. PDE5s.and post-menopausal women son with other studies is not possible. however. as well as drugs that response in women. 109–111]. However. 106].. Hence. the women with demonstrated low vasocongestive sexual response effects of the pharmacological response (as indicated by VPA) [107]. Specifically. The majority of this research inhibit adrenergic-mediated vasoconstriction has investigated the utility of dopaminergic processes (e. apomor- order. majority of these studies have found that while whereas Alprostadil (a vasodilator) [111] and sildenafil may produce increases in genital vaso. and may be of benefit to women with can- cer who are experiencing sexual side-effects as a While the majority of human research on result of medication use. desire or satisfaction [105. they had no significant effect on subjec. rotransmitter agonists or antagonists) on sexual Zestra.e. indicated by VPA) in pre. Hence. orgasm. phen. Alprostadil cream).. and ephedrine increased vaginal congestion (as however. Finally. yohimbine.

adrena. the risks of prescribing the use of a suction device that increases blood hormonal agents for women with cancer must flow to the clitoris. tablets or rings data seems to suggest that women’s experiences may be recommended on a short term basis of arousal are determined more by changes that [104]. postmenopausal women with vaginal atrophy or pret discrepant results. EROS therapy involves difficulties in women. and has been demonstrated be carefully weighed against the possibility of to be beneficial in reducing arousal disorder increasing the amount of circulating hormones. there are currently some initiatives nature of the relationship between testosterone underway to investigate the relationship between and sexual response is not well understood sexual arousal and other neurotransmitter sys. tems (e. The majority of research while some research suggests that dopaminergic suggests that estrogen has little direct impact on and noradrenergic agents may facilitate sexual sexual desire or subjective arousability. As with testosterone therapies. and very While there are currently no randomized con- few of these studies have made concurrent use trolled trials of psychological interventions spe- of psychophysiological measures of arousal cifically designed for the treatment of arousal (such as VPA or thermal imaging). Karvinen and colleagues found remains questionable [85]. there is research suggesting the . the use of hormones to cise guidelines demonstrated significantly bet- ameliorate symptoms of FSAD have been based ter results regarding sexual functioning. and methodological differences shown it to be successful [116]. Few controlled studies currently treating surgically menopausal women have not exist in women. arousal. lubrication and satisfaction [117] others have found no benefit at all [118]. image and fatigue than those who were seden- 93]. subjects found no impact on arousal at all [115]. Given that the available vulvar disease. while disorders [122]. and stud- arousal in women. receptor positive cancers [119]. Additional biological interventions for cancer patients: while all of the above may be consid- Hormonal Agents ered for alleviating symptoms of sexual arousal disorder in women with cancer. Even in non-­ that cancer patients who met public health exer- oncology populations.g. Overall. [116]. estrogen creams. the role of line. the Finally. norepinephrine. 116]). which must be evaluated when pre- mechanisms underlying experiences of female scribing their use in women with estrogen-­ sexual arousal seems highly necessary. however. symptoms and significantly improving FSFI especially since the extent of improvement in scores in women with cervical cancer [120]. arousal and satisfaction in some women. desire. but the evidence is far from systemic estrogen in improving sexual arous- conclusive (for a review see [38. and opioids). sexual functioning from hormonal therapies Additionally. While some of these studies have found tary [121].. this finding is based on highly ies examining the efficacy of estrogen alone in limited data. two additional While androgen and estrogen therapies have treatments have also been examined: EROS been examined as treatments for sexual arousal therapy and exercise. recent research suggests that occur ‘mentally’ than by changes that occur these treatments can increase circulating levels genitally. serotonoin. Thus. body on highly limited and conflicting research [38. a recent controlled there is evidence indicating that testosterone study testing the impact of Levadopa in healthy treatment may be effective in increasing desire.10  Disorders of Female Sexual Arousal 139 arousal and orgasm [114].Psychological Interventions ies have provided only brief tests of testoster- one treatment in estrogenized women. ability is also unclear. It is important to note that most of these stud. In estrogenized between these studies make it difficult to inter. a surge in research on the neural of estrogen. general improvements in sexual responsiveness.

In some cases. however. individual psychological treat. crepancies in sexual scripts/expectations) that may be contributing to the woman’s arousal dif- ficulties. that the most effective educa- and female sexual response. examining the impact of the above therapeutic tive distraction during sexual activity. dis. relationship sat- myths/distortions.. ing patients with reading material. anxiety. Persistent Genital Arousal Disorder gies can help the couple work through their sex- ual and relational difficulties. communication. standard behavioral and communication strate. mood/distress. arousal difficulties. cou. intimacy following cancer diagnosis. When working with cancer patients. While there is no tions of sexuality and intimacy within the context mention of PGAD in the DSM-IV-TR. resolve with orgasm and are not necessarily trig- course. relatively low cost way to educate individuals on depression.g. 130]. body image dissatisfaction) some of the more common sexual side effects of interacting with the arousal difficulty. and cognitive restructur. In addition to individual psychotherapy. an of chronic illness. gered by sexual activity [131]. However. highlighting the importance tioning the genital area following radiation or sur. these through psychotherapy. that exist have focused specifically on disorders the impact of past sexual experiences (particularly of desire or orgasm. Treatment cancer and how to deal with them. and the techniques on sexual functioning. provid- cess. contextual influences on sexual arousability (e. Finally. There are currently very few outcome studies the detrimental effects of negative affect or cogni.g. such ­international consultation on women’s sexual as sensate focus. as opposed to arousal (for an sexual trauma) may need to be directly addressed exception. of having reading material that targets specific gery. .. these physical sensations do not may not necessarily be to re-initiate sexual inter. Relaxation- techniques targeting the individual or relational based or mindfulness training can facilitate the difficulties identified in the clinical interview pro. Sarin benefits of psychoeducational interventions for education that is tailored to the patient’s cancer female cancer patients with FSAD [123–126]. see [127]). subjective adaptive sexual attitudes/beliefs. can aid in teaching couples about the sexual Psychological interventions typically incorporate changes that have occurred in the patient’s body a combination of general cognitive and behavioral and how best to deal with them. orgasm. It is important for Persistent genital arousal disorder (PGAD) is a the therapist to work with the couple to identify syndrome characterized by high levels of spon- their goals when dealing with FSAD. and problems and specific populations [128]. dilatation exercises tional pamphlets are ones that are tailored to the and pelvic floor musculature exercises for condi. but rather to broaden the couple’s defini. sexual arousal.140 T. For the most part. the goal Furthermore. As mentioned earlier. can help the couple to begin functioning recognized that a number of women body exploration. ple therapy is also recommended to address particularly regarding the efficacy of individual issues in the relationship (e.g. more controlled research in this area.M. trials have indicated general improvements in ing techniques may be employed to modify mal. such as infor- ment may involve brief interventions to specifically mation pamphlets or lists of resources is a address comorbid mood disturbances (e. individual’s needs. Sex toms that has come to be known as PGAD [13]. Research sug- may also include psychoeducation about cancer gests. and to taneous and unwanted genital arousal that occurs determine what their need is vis-à-vis increased in the absence of sexual interest or desire [131]. 129. expectancies and arousal. Kukkonen and S. psychotherapy treatment components in treating trust.. experiencing of pleasure [127]. and increase communication suffer from a particular constellation of symp- and appreciation of pleasurable sensations. self-reported levels of sexual desire. is desperately needed. For example. and the few need for appropriate erotic stimuli). isfaction and overall well-being [127. Sex therapy techniques. effective stimulation techniques.

arousal. Cause of persistent genital arousal is unknown. partner variables and relationship Panic attacks functioning. a lack of physiological measurement of toms.  10. Involuntary genital or clitoral arousal that studied in an oncology population. the overlap between arousal disorders and those case examples. pelvic ­massage.4  Clinical correlates of PGAD assessment be conducted that examines physio- Chronic fatigue logical issues such as cancer treatment and med- Depression ication use. or small pilot studies [133–139] of desire and orgasm and future diagnostic sys- (See Table 10. such as SSRIs. and poor control over to cause priapism in some men [131]. as presented by Krychman et al. faceted problems that are only beginning to be ful of research that exists on risk factors and understood. et al. there has been no attempt The research on female sexual arousal in cancer to systematically study treatment for women with patients is limited and our understanding is PGAD. which women ate between physiological and psychological have reported to induce or relieve their symp. tems will likely collapse the categories into one. Anecdotal reports suggest monitoring clouded by questionnaires that do not differenti- medication use. [140]. variables that interact with arousal difficulties. cant proportion of female cancer patients suffer however. social support groups and mood. [141]).10  Disorders of Female Sexual Arousal 141 Leiblum and Nathan [132] were the first to with no empirical evidence to back up these describe PGAD and listed five features that have claims [131]. there are no prevalence estimates on Disorders of female sexual arousal are multi- PGAD in the general population and the hand. Genital arousal is unrelated to feelings of tional cell carcinoma as presented in DiGiorgi sexual desire. as well as psychological function- Increased vaginal vasocongestion ing.g. 5. Despite these limitations. Genital arousal is associated with moderate levels of distress. At present. Physiological genital arousal does not resolve toms. In dealing with patients who complain of arousal difficulties. They were also careful to distinguish PGAD from hypersexuality by the key component of Conclusion a lack of sexual desire or mental sexual arousal. depending on the type of cancer and with one or more orgasms. In addition. Current conceptualizations highlight etiology is entirely based either on self-report. While PGAD has never been 1. multiple psychological. or high grade anaplastic astrocytoma 4. relational and physical life-style changes.3 for treatment summary). Pelvic varices The study of sexual arousal disorders in women Neuropathy is still in its infancy and clearly. transi- 3. Treatment options can vary from broaden- Clitoral pain Overactive bladder syndrome ing the patient’s definitions of sexuality and Restless leg syndrome sexual activity. this is a disorder that requires more disorder: systematic study regarding its prevalence. to adjusting or prescribing differ- Hypersensitivity of urethra ent medications to ameliorate genital vasocon- Hypersensitivity of genital area gestion (see Fig. become the standard diagnostic criteria for this Clearly. treatment that they are receiving (e. able that some patients could exhibit these symp- 2. cognitive-behavioral therapy. it is clear that a signifi- stabilizing medications have been suggested. or trazadone. which has been demonstrated arousal in cancer patients.4 for correlates of PGAD). there are many . etiol- ogy and treatment. this is all based on single case examples from sexual arousal problems.. it is conceiv- persists for an extended period of time. it is recommended that a full psychosexual Table 10. To our knowledge.

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Cancer and Sexual Health. text revision (DSM- IV-TR) [1]. also specify that the diagnosis of FOD should be ing severity of the disease. access to social support. Orgasms have been how they pertain to women with current or past reported to be induced by erotic stimulation of cancer. or mons. Research indicates that stimulation of cancer survivors. A few cases cancer and its treatment can impact orgasm and of spontaneous orgasm without an obvious source sexual functioning at large is also provided. an’s orgasmic capacity is less than that would be nosis and management. TX 78712. where possible. defines FOD as the persistent or Both cancer and cancer treatments can have recurrent delay in. and is glans. sexual experience. LLC 2011 . periurethral sexual response in both men and women. Khouri. treatment intensity based on the clinician’s judgment that the wom- and length. of sexual stimulation have been reported in the lit- erature [6. prevalence. In this adequacy of sexual ­stimulation she receives. orgasm. Meston (*) Department of Psychology. with an emphasis.). orgasm ­following ­deleterious effects on women’s ability to attain a normal sexual excitement phase. the context in which the disturbance C. 147 DOI 10. and Cindy M. Spontaneous orgasms have also been reported with the use of antidepressants [8–10]. via mental imagery. and social factors includ. situational). The degree to which sexual functioning the disturbance must cause marked ­distress or at large is impacted depends on a number of interpersonal difficulty. fourth edition. emotional status during cancer diag. It is important to note that the type or intensity and treatment of female orgasmic disorder of sexual stimulation required for obtaining orgasm (FOD). 3]. psychological. on varies widely across women. or absence of. we discuss the diagnosis. or fantasy. the FOD is a result of psychological or ­combined Austin. acquired). In addition. (eds. Most studies refer to orgasm problems in J. 1 University Station A8000. Current Clinical Urology. Corey Pallatto Hughan. University of Texas occurs (generalized vs. The DSM-IV-TR subtypes are used to ­indicate the onset of orgasmic disturbance (lifelong vs. 5].M. Definitions of Female Orgasm cations • Sex therapy Disorder The Diagnostic and Statistical Manual of Mental Introduction Disorders. in addition to the clitoris and affected frequently in humans from the studies vagina [2. 7].1007/978-1-60761-916-1_11. and the and comorbid psychological problems.P. reasonable for her age. Mulhall et al. © Springer Science+Business Media. The diagnostic criteria medical. USA factors. Orgasm is a fundamental component of genital areas such as the breast/nipple. Meston Keywords  Orgasm • anorgasmia • SSRI medi. and hypnosis has A summary of the specific ways in which been shown to induce orgasm [4. and whether at Austin. chapter.Chapter 11 Disorders of Female Orgasm Yasisca P.

tion but not with intercourse alone would not orgasmic dysfunction is an absence of. a DSM-IV-TR at least 6 months. Orgasmic problems were noted by 29% of orgasm must follow a normal sexual excitement women (aged 18–73) who attended an outpa- stage produced by adequate sexual stimulation. Women who were initially orgasmic but later obtain orgasms Orgasm difficulties ranked as the second most infrequently and women who achieve orgasms in frequently reported sexual problem after sexual only certain contexts. tient gynecologic clinic [16] and by 23% of Thus. According to the DSM. The World Health Organization’s Inter- Although situational FOD is understood to national Statistical Classification of Diseases mean that orgasm difficulties occur in specific and Related Health Problems. subtype). A large proportion of women who meet FOD Specifically. DSM-IV-TR cri. markedly diminished intensity of Secondary orgasmic dysfunction relates to orgasmic sensations. with certain types of sexual desire difficulties based on the interviews of activity or with certain partners are examples of 1749 American women (aged 18–59) in the the heterogeneity found with secondary FOD. a diag- The Prevalence of Female Orgasmic nosis of secondary orgasmic dysfunction (acquired and/or situational FOD) encompasses a Disorder wide range of clinical presentations. women as either primary orgasmic dysfunction not achieved. unless edly delayed. Khouri et al. A recent study of attendees arousal is achieved. the lack of orgasm is due to FSAD. If the that keep the individual from participating in disorder does not cause the women marked dis. [17] ­suggested the follow- primary orgasmic dysfunction was introduced ing revised FOD definition in order to address the by Masters and Johnson [11] and has been used fact that a DSM-IV-TR diagnosis of FOD pre- to describe women who report never having cludes one of female sexual arousal disorder. but this is not always the case. preceding the anorgasmia: “despite the self-report IV-TR. lack of orgasm. contexts. 25% reported a lack of orgasm in diagnostic criteria also meet the criteria for female the past year for at least ­several months or more. National Health and Social Life Survey [82]. 10th Revision. sexual arousal disorder [14–16]. without ­subtypes. women with comorbid FSAD and FOD women (aged 18–65+) attending a UK general may indeed have orgasm difficulties when sexual practice clinic [18]. the clinical consensus is that achieving defines orgasm dysfunction in broader terms and orgasm during intercourse with manual stimula. or marked delay of orgasm women who meet criteria for acquired and/or from any kind of stimulation. If adequate sexual arousal is (aged 18–75) at several general practice clinics .” situational FOD. Other criteria capability as a problem nor do they report include frequently occurring orgasm difficulties ­experiencing significant distress [12. This percentage is comparable to clinic-based teria explicitly state that the absence or delay in data. this would refer to those women who of high sexual arousal/excitement. While lifelong. and must not be the result of prolonged ceive their anorgasmia or reduced orgasmic abstinence from sexual activity.P. there is either meet criteria for lifelong and generalized FOD. also to highlight the need for adequate arousal including masturbation. generalized FOD is a clear diagnosis covering all sexual situations. orgasm in which the individual has ­clinically significant distress is present. or mark- meet criteria for clinical diagnosis. and experienced orgasm under any circumstances. ­satisfactory sexual activity lasting for a period of tress or interpersonal difficulty. The term not FOD. Basson et al. The had no experience of an orgasm in any situation inability to achieve orgasm when one wishes (similar to “lifelong” subtype in DSM-IV-TR) or may result in sexual distress or dissatisfaction in developed the dysfunction after a period of rela- women. Some tively normal response (similar to “acquired” women meet criteria for FOD and do not per.148 Y. or secondary orgasmic dysfunction. 13]. diagnosis of FOD is not given. According to the ICD-10.

As they battle 82]. which can negatively affect sexual cancer reported sexual problems as having a functioning. and sexual functioning is particularly pleasing for them. for example. and vagina [20]. sexual dys. the brain for stimuli [26]. through the administration of selective serotonin . interest and desire [28]. [82] found that the ­frequency of orgasm both with a partner When a woman is diagnosed with cancer. one’s life can induce feelings of anger. but has a high patient survival rate – 75% live at weight gain. many basic human processes are with their bodies and learn what is sexually affected. the fact that most studies report the impact on Symptoms such as pain during intercourse can sexual functioning in general without specifi. but cross-study compari. is certainly more than skin deep. while disfiguring son has proved to be difficult as patients fall into ­surgeries can alter a patient’s self-image as a different categories of diagnoses. ­illness. ovaries. premature meno- cancer diagnosed in women and inherently inter. Schover and Jensen elucidate the relation- tion in cancer survivors is complicated by the ship between the two by asserting that cancer and diversity of psychological. ­frequency may be due to differences in sexual When treating an oncological patient. stages. Patients may also face arousal of the cancer [23]. Other possible sexual Gynecological cancer is the third most common side effects include genital pain. In their book about sexuality and chronic Evaluating the prevalence of orgasm dysfunc. gynecological cancer reduced vaginal elasticity [27]. As young women engage in more sexual their ailments. and guilt. fallopian In addition to physical effects. lead to an initial diagnosis. pause. Age differences in orgasm be done to give her the best possible prognosis. vomiting. they may become more familiar of side effects. patients often cope with a variety experiences. situations that would normally diagnosis. 50% of women with gynecological ­disorder. can affect the cervix. and sexual being and lead to a decrease in sexual treatments [22]. fear. 13% of which reported Sexual Health it was also a problem for them [13]. uterus. including how to achieve susceptible to complications. and concern about cally addressing orgasm dysfunction. vaginal dryness. medical. however. endometrium. Potentially losing studies have examined sexual dysfunction result. Patients recovering from function is a serious issue for cancer survivors. ­anxiety. the and ­during masturbation was greater for older priority for medical professionals is to determine groups of women and lowest for women between whether or not she will survive and what must 18 and 24 years of age. side effects such as hair loss. Several also suffer emotional trauma. patients may tubes. sadness. and fatigue. cancer may face depression and adjustment in one study. patients must cope with the most common cancer diagnosed in women. the main experience such that younger women tend to focus is on the physical ailment. roughly half the survivors exhibited a excite someone may not elicit the same effect decreased interest in sex while 30% reported a because chemotherapy affects the chemicals of decrease in sexual activity overall [22]. cancer have less experience and fewer partners [19. and this can be further compounded ­devastating impact on quality of life [24]. and social its associated treatments can affect all biological factors that contribute to sexual outcomes and by systems necessary for normal sexual function. Breast cancer is eradicate cancer cells. orgasm.11  Disorders of Female Orgasm 149 revealed that 18% received an ICD-10 diagnosis The Impact of Cancer on Women’s of orgasmic dysfunction. gynecologic cancers. Although surgery. chemotherapy. and radiation term sexual dysfunction [20]. least 5 years post-diagnosis [21]. ing from these cancers. and vaginal feres with sexual functioning due to the location stenosis [22]. Despite this issue. nausea. In a study of Sexual responses are also affected by treat- breast cancer survivors 1–5 years after initial ment. one half experience long. Defined as cancer of the problems due to decreased lubrication and female reproductive tract. Out of the their sexual functioning can influence patients as population of women treated for breast and they evaluate possible treatment options [25]. dyspareunia.

but no have revealed that sexual dysfunction can be a differences in orgasmic function or dyspareunia side effect of SSRIs. that women who underwent ­chemotherapy were vic surgery often results in changes to sexual seven times more likely to report difficulty functioning along with one’s body image and attaining orgasm than women not treated with self-esteem [32]. a common side effect of chemotherapy. diabetes. and decreased sexual activity literature. Radiation-induced injury to genital organs must be shouldered by their partners. Relationship issues may also develop during Radiation can cause thickening and contraction a cancer diagnosis and therapy. need to reduce their workload in order to fully and changes in texture leading to difficulties recuperate. ual functioning. 83]. [34] found that women after chemotherapy. 26% reported sexual dysfunction arousal.. determine what impacts the patient’s sexuality: Radiation therapy impacts orgasm function to the cancer treatment or SSRI [29]. Ovarian failure due to chemother- chemotherapy. negatively apy is considered to have a direct effect on sex- impact sexual functioning and satisfaction. Head. women treated with radical ism) and is commonly used for treating estrogen pelvic surgery were found to have less sexual receptor positive breast cancer [32]. Although invasive treatments [42]. [39] noted that in a ­sample as the woman recovers can create marital and of 118 women with cervical or vaginal cancer. change [83]. Thakar et  al.g. Sexual rehabilitation may be orgasm 1 month after radiotherapy with little required for the couple to return to their previous improvement at 1 year (62%). sexual tension that further damages the couple’s 67% reported never to occasionally experiencing relationship [30]. 83]. the levels of intimacy. Combining two or more therapies can result in provided by the ovaries. such as surgical procedures. may impact the way a woman feels about her Women with cancer often face issues with their sexual attractiveness and self-esteem [32. so it may be difficult to at 12 months p­ ost-surgery [35]. In addition. Young-McCaughan [41] reported elasticity.150 Y. High costs has been reported objectively [36] and subjec- of medical care may also impose a financial bur. is associated with even greater sexual dysfunction via vaginal decreased vaginal lubrication leading to diffi- stenosis. mies on orgasm frequency. Endocrine therapy is effective for several quency. vaginal stenosis.5 times greater for women with cancer compared to the control group. Selective . loss of ties [40. radiation. tively by patients [37. known as the narrowing of the vagina culty with intercourse and other sexual activi- accompanied with increased dryness. Studies desire and decreased vaginal ­lubrication. a greater degree than does the pelvic surgery. face. intercourse fre. 38] described in the cancer den on the couple. and hormone therapy. 12 from women who received partial hysterecto.P. Undergoing pel. 66% of women chemotherapy. or genital hair Treatments on Orgasm Function loss. When compared to medical conditions (e. or sexual desire. relative risk of orgasm dysfunction was approxi- mately 1. which can seriously strain a relation. In one study. a decrease in estrogen levels. with vaginal penetration and genital sensitivity ship as their domestic and wage-earning duties [32]. sexual health as procedures designed to treat Other side effects include fatigue and weight cancer. Women may of the skin in the vaginal canal. Results from an outpatient study treated with radical pelvic surgery continued to of 50 Italian women emphasize the damaging experience sexual problems more than 6 months effects of chemotherapy compared to other after the surgery [33]. and scar tissue [31]. and 6% respectively [42]. reuptake inhibitors (SSRIs) as treatment. Khouri et al. Chemotherapy is particularly detrimental to Effects of Specific Cancer orgasmic function. Of the women who did not ­surgeries such as hysterectomies may affect the report sexual problems prior to breast cancer autonomic nerves ­activated during sexual treatment. much greater than the receiving full hysterectomies did not differ women treated with surgery or radiotherapy. Jensen et al. hypothyroid- healthy controls.

11  Disorders of Female Orgasm 151

estrogen receptor modulators such as tamoxifen Psychological Approaches (Table 11.1)
and raloxifene bind to the receptor sites within
cancer cells not allowing the cell to divide.
Directed Masturbation
Other hormone treatments include aromatase
inhibitors and GnRH agonists, which lower
For women with orgasm dysfunction, masturba-
estrogen levels. One prospective study of women
tion exercises may be beneficial in a number of
receiving different combinations of hormone
ways. Focussing on nonsexual cues rather than
therapy found that women reported minimal
sexually arousing cues has been shown to impair
sexual side effects with the use of tomaxifen
sexual response [44]. Masturbation can help
alone and significant sexual dysfunction with
guide a woman’s attention toward pleasurable
zoladex, a luteinizing hormone-releasing hor-
sexual sensations (i.e., erotic cues). In addition,
mone agonist, compared to cancer patients not
solitary masturbation eliminates performance
receiving endocrine therapy [43]. Generally,
anxiety or discomfort with communicating with a
cancer patients tolerate endocrine treatment
partner, both of which may play role in a ­woman’s
much better than other therapies, especially che-
orgasm difficulties. Moreover, having the ability
motherapy (e.g., [32]).
to immediately adjust the type of stimulation and
intensity according to what a woman prefers may
be more effective than depending on her partner
to touch her with appropriate stimulation.
The Treatment of Female For women with primary anorgasmia, directed
Orgasmic Disorder masturbation is the most frequently prescribed
treatment. This treatment program was initially
Several therapeutic perspectives including psy- developed by LoPiccolo and Lobitz [45] and other
choanalytic, cognitive-behavioral, pharmacolog- researchers have produced variations of directed
ical, and systems theories approaches have been masturbation such as bibliotherapy, individual,
applied to the treatment of anorgasmia. To our couples, and group therapy formats (e.g., [46]).
knowledge, there has been little research on the The directed masturbation program consists of
effectiveness of these interventions specifically successive stages of guided masturbation to train a
among cancer survivors who experience orgasm woman to locate and manually stimulate genital
difficulties. Cancer survivors face a number of areas that bring her sexual ­pleasure. The first stages
psychological and physiological challenges that begin with a visual examination of her body, using
need to be considered when planning treatments a mirror and ­educational diagrams depicting female
for sexual concerns. Here we review the effec- genital anatomy. After visual and manual identifi-
tiveness of empirically validated treatments for cation of her genitals, she is instructed to explore
orgasm difficulties. Where available, we include those areas and note which genital areas are sensi-
information on whether the treatment has been tive and elicit pleasure. Then she is instructed to
effective among cancer survivors. apply targeted manual stimulation to these regions
Determining a course of treatment for sexual and to increase the intensity and duration until
dysfunction in cancer patients requires addi- “something happens” or until discomfort arises.
tional research and investigation as sexuality Aids such as topical lubricants, vibrators, and erotic
issues are not frequently discussed during rou- materials can be incorporated into the exercises.
tine oncological care [84]. The addition of sexual Training on self-stimulation is directed toward the
health training for physicians and improved woman’s achieving orgasm alone. Once she has
patient education detailing cancer’s potential accomplished this, her partner is included in the
sexual side effects would ensure a more accurate directed masturbation sessions. The addition of her
prevalence assessment and hopefully break down partner’s presence serves as desensitization to anx-
communication barriers between patients and iety that she may have experienced up until this
physicians. point. As the woman learns to experience sexual


Table 11.1  Studies for the psychological treatment of orgasm dysfunction
References Design N Treatment Conclusion Level of evidence
Directed masturbation (DM) studies
LoPiccolo and Lobitz [45] Single group 8 women with Individual DM All subjects, orgasmic Assessment method not specified
treatment study; primary modeled after with masturbation,
15 sessions anorgasmia Masters and 75% coitally
Johnson, combined orgasmic; gains
with Kegel maintained at 6-month
exercises follow-up
Barbach [49] Single group 83 women with DM in group therapy 92% of subjects orgasmic Anorgasmia defined as no orgasmic
treatment study; primary with masturbation experience
10 sessions over anorgasmia
5 weeks
Heinrich [50] Randomized 44 women with DM in group therapy Both DM treatments Assessment method not specified
three-leg study primary (10 sessions/5 improve masturbatory
with control anorgasmia weeks) vs. and coital orgasmic
condition; individual DM function (with group
between 1 and 5 bibliotherapy (1 therapy more
weeks in length session) vs. wait effective); little to no
list improvement with
wait list
McMullen and Rosen [52] Randomized 60 women with DM with videotape No significant difference Sexual function questionnaire,
three-leg study primary modeling vs. DM between DM clinician interview, self-reports
with control anorgasmia with written conditions, but both
condition; 1 instruction vs. wait more effective than
session weekly list wait list; gains
for 6 weeks maintained/improved
at 1-year follow-up
Delehanty [51] Randomized 28 preorgasmic DM and assertiveness 82% of subjects achieved Sexual function questionnaire,
two-leg study women training in group orgasmic success with self-reports
with control therapy for 10 treatment
condition; weeks vs. wait list
Y.P. Khouri et al.

Fitchen et al. [53] Randomized 23 women with DM, sexual info, No change in orgasm for Subjects orgasmic less than 25%
three-leg study; secondary relaxation, Kegel all groups of time
14 week anorgasmia exercises, sensate
duration focus, sexual
training; done with
couples vs. groups
vs. minimal contact
Hurlbert and Apt [54] Randomized 36 women with Individual coital CAT subjects improved Self-reports and sex diaries
two-leg study; secondary alignment more substantially in
11  Disorders of Female Orgasm

four treatment anorgasmia technique (CAT) coital orgasmic
sessions and vs. individual DM function than DM
four phone subjects
No control outcome studies
Masters and Johnson [11] Single group 342 women with Couple’s therapy that Varying levels of Assessment method not specified
treatment study primary and included sex improvement for all
secondary education, sensate subjects; 1–2%
anorgasmia focus, sex relapse rate at 1-year
communication follow-up
training, and
in vivo systematic
Brotto et al. [27] Single group 26 women seeking Mindfulness-based Improvement in Clinician assessment
treatment study; treatment for psychoeducation subjective feelings of
three sessions/6 acquired sexual (PED) in small wetness post-PED
weeks desire and/or groups (4–6 compared to baseline;
arousal concerns women) beneficial effect on
sexual desire and

154 Y.P. Khouri et al.

arousal and orgasm openly in the company of her number of orgasms during sexual activity with
partner, anxiety accompanying sexual encounters their spouse after four 30-min sessions. The ben-
lessens. In addition, the partner is able to observe efits of this technique result from the fact that cli-
how to stimulate the woman effectively. toral contact and possibly paraurethral stimulation
Directed masturbation is highly effective and are maximized. The effectiveness of directed
evidence to support this treatment is presented in masturbation for the treatment of anorgasmia
the link between masturbation and orgasm ­ability. among cancer survivors has yet to be examined.
Kinsey et al. [47] reported that the average woman
reached orgasm more frequently during masturba-
tion than with intercourse (95 vs. 73% of the time). Anxiety Reduction Techniques
More recently, Laumann et  al. [48] reported a
strong relation between frequency of masturba- Barlow [44] theorized that when faced with a sex-
tion and orgasmic ability during masturbation. ual situation, individuals with sexual dysfunction
Women who masturbated one to six times per year shift their focus of attention away from erotic cues
reported less frequent orgasms (67%) than women and re-direct their attention toward nonerotic cues
who masturbated once a week or more (81%). (e.g., performance anxiety). This may be particu-
A number of outcome studies and case series larly relevant for cancer survivors as their bodies
reported directed masturbation is highly success- can be changed physically through the treatment
ful for treating primary anorgasmia. High rates of cancer. During sexual situations, these women
have been reported for orgasm attainment may begin to focus on body image concerns stem-
through group directed masturbation, ranging ming from altered breast [55] or genital tissues
from 82 to 100% of anorgasmic women [49–51]. [56]. Healthy women with orgasm dysfunction
Self-directed masturbation via text and video may experience anxiety and negative emotions
yielded lower rates, 47–65% [50, 52]. such as performance concerns, embarrassment, or
Few controlled studies have examined the guilt. It is very likely that cancer patients might
effects of directed masturbation for treating also experience negative effect regarding impor-
­secondary anorgasmia. Fitchen et  al. [53] com- tant issues such as mortality and loss of reproduc-
pared minimal therapist contact bibliography tive capability [28] that could result in orgasmic
with several established techniques, including ­difficulties along with other sexual problems.
directed masturbation, relaxation exercises, Kegel Focussing on these and other anxieties and
exercises, sensate focus, and sexual ­communication ­concerns could result in “spectatoring” or self-
training. Surprisingly, the authors found no monitoring during sexual activity [11]. Spectatoring
change in orgasmic ability among 23 women with is thought to impede sexual functioning through
secondary anorgasmia. These findings may indi- cognitive interference, with cognitions being
cate that factors other than orienting oneself to directed away from the sexual experience and
her body sexually and focussing on pleasurable leaving less cognitive resources for processing
physical sensations may be at play. Hurlbert and erotic and physiological arousal cues.
Apt [54] compared the effectiveness of directed Two commonly prescribed anxiety reduction
masturbation with coital alignment technique in techniques for the treatment of FOD include
36 women with secondary anorgasmia. Coital ­systematic desensitization and sensate focus.
alignment is a technique in which the woman Wolpe [57] developed systematic desensitization
assumes the supine position and the man posi- for the treatment of specific phobias. When
tions himself up and forward on the women. applied to orgasmic dysfunction, the woman and
Thirty-seven percent of the women and their the therapist create a fear hierarchy of anxiety-
spouses receiving instructions on coital alignment provoking stimuli which successively increases
technique vs. 18% of those receiving directed in the amount of anxiety the activity produces.
masturbation reported substantial improvements The deep relaxation exercise training aids in
(>50% increase) in orgasmic ability during inter- replacing fear responses with a calm, relaxed
course, orgasmic strength, and an increase in the state. When anxiety is reduced and a relaxed state

11  Disorders of Female Orgasm 155

is achieved, the woman can ­progress to the next, Other Techniques
more fearful task in the hierarchy. The procedure
is first completed by imagining all the items on Sex education has been an important component
the hierarchy. Afterward, she restarts the fear of sex therapy since the publication of Masters
hierarchy by engaging in the actual activities. and Johnson’s Human Sexual Inadequacy (1970).
Sensate focus is a skills-based couples’ ­therapy Particularly, education about genital anatomy and
developed by Masters and Johnson [11] that, like learning techniques to enhance sexual pleasure
directed masturbation, increases awareness of aid in gaining orgasmic capability. Several studies
sexually pleasurable regions for each partner and provide evidence for the effectiveness of sexual
emphasizes communication of each other’s education for primary and secondary anorgasmia
­preferences and pleasurable experiences via a [61]. [27] examined the effects of a brief sex
sequence of body-touching exercises. The first education intervention on sexual arousal con-
stage of sensate focus is to explore their partner’s cerns among women with early-stage gyneco-
nonsexual body areas without the goal of sexual logic cancer. The sexual education was conducted
activity. Once the couple increases the practice of over three 1-h sessions and included education
sexual touching without the pressure of inter- on masturbation and orgasm attainment, marital
course and the woman can maintain a relaxed satisfaction, mindfulness, and relaxation tech-
state, she can move toward more sexually ori- niques. Among improvements in sexual func-
ented touching such as female-guided genital tion, orgasm frequency and satisfaction increased
stimulation or penile stimulation and eventually ­significantly after the intervention.
intercourse. Sensate focus combines the hierar- Kegel [62] proposed that conducting ­exercises
chical nature of systematic desensitization with that strengthen the pubococcygeous muscle
in vivo desensitization in order to reduce anxiety could facilitate orgasm by increasing vascularity
associated with orgasm performance. to the genitals. Treatment studies comparing
Many of the treatment outcome studies that therapies with and without Kegel exercises have
assess the effectiveness of anxiety reducing not produced significant differences in the alle-
­techniques for FOD combine these techniques viation of orgasmic dysfunction. However, Kegel
with other modalities such as directed masturba- exercises may act to boost orgasmic ability by
tion, skills and communication training, biblio- enhancing physical arousal via increasing vascu-
therapy, Kegel exercises, or sexual education. With larity in the pubococcygeous muscle and may
the current literature, it is difficult to ascertain the help women to identify and focus on pleasurable
extent to which these anxiety-focussed modalities genital feelings much in the same way as other
impact treatment outcomes. In addition, the varia- genital stimulation techniques.
tion in sample characteristics, such as demograph-
ics, sexual dysfunction severity, diagnoses, primary
vs. secondary anorgasmia, therapist characteris-
tics, and treatment setting and duration, provides Pharmacological Approaches
additional heterogeneity when systematically
comparing anxiety reduction techniques. Meston A small number of placebo-controlled studies
et al. [58] reviewed controlled studies and found have examined the effectiveness of pharmacologic
that anxiety appears to play a small role in FOD agents for treating FOD not induced by antide-
and these techniques are most effective when pressant medication. Sustained release bupropion
women experience concurrent sexual anxiety. failed to improve orgasm in nondepressed, anti-
Cancer patients use relaxation techniques to reduce depressant-free women (n = 20) with orgasmic
general anxieties [59]; it may be possible that sex- dysfunction as compared to placebo [63]. However,
ually anxious individuals could benefit from such a small percentage of women (20%) experienced
techniques. Sexual anxiety was found to be a key facilitated and/or more intense orgasm during
factor in sexual relationships of women after breast bupropion treatment. Zajecka et al. [64] reported
reconstruction surgery [60]. improvement in orgasm among depressed women

156 Y.P. Khouri et al.

reporting sexual dysfunction, including orgasm primarily consisted of either estrogen or androgen
difficulties, compared to baseline after 12 weeks therapy [32, 69]. Cancer treatments such as
of treatment with nefazodone. Studies on sildena- chemotherapy and hysterectomies may lead to
fil for FOD show mixed results. In one study, 53 impaired ovary function [85]. Ovarian failure
premenopausal women diagnosed with sexual results in decreased levels of androgens and
arousal disorder received a randomized combina- estrogen which, in turn, can impair sexual func-
tion of three 4-week periods consisting of either tioning, particularly sexual arousal [70]. Much
sildenafil, or washout, or placebo [65]. Women of the hormone replacement research is dedi-
reported improvements in sexual arousal and cated to the alleviation of menopausal symp-
orgasm and increased frequency of sexual fanta- toms, natural and chemotherapy-induced, which
sies and intercourse with sildenafil [65]. These include changes in one’s sexual function (for a
findings were replicated in premenopausal women review, see Hickey et al. [71]).
with sexual arousal disorder and type I diabetes A case series conducted by [84] found that
[66]. An in-laboratory study by Basson and Brotto oral esterified estrogen with methyl-testosterone
[67], however, found that the administration of (known commonly as the testosterone patch)
sildenafil (Viagra) among 34 postmenopausal improved sexual desire and arousal in three
estrogenized women did not improve sexual women with a history of recent breast cancer,
arousal or orgasm. Meston et  al. [68] examined one of which reported an increase in orgasmic
the effects of Ginkgo biloba in 68 sexually dys- function. Although hormone treatment has been
functional women. Women were randomly shown to be effective and well tolerated (e.g.,
assigned to 8 weeks of Ginkgo biloba extract, sex [72, 73]), certain risks have been identified.
therapy, placebo, or Ginkgo biloba combined with Findings from the Women’s Health Initiative
sex therapy. Long-term use of Ginkgo biloba alone conducted across 40 US clinical sites conserva-
did not have a significant impact on sexual func- tively suggest that hormone therapy may be
tioning, though when combined with sex therapy, linked to increased risk of heart disease and
significant increases were noted for sexual desire stroke and that beginning hormone therapy closer
and satisfaction compared to placebo. Sex therapy to menopause decreases the risk of heart disease
alone significantly increased orgasmic function. [73–75].
Several studies have examined potential Complementary and alternative treatments
­pharmacotherapies for treating FOD induced by are used by cancer patients primarily to alleviate
medications such as SSRIs, antipsychotic, and symptoms and side effects due to the disease
antiepilepsy drugs. Drugs tested as antidotes itself and conventional treatment. Several survey
include antiserotonergic agents, such as cypro- studies have found that usage rates range from
heptadine, buspirone, mirtazapine, and granise- 9  to 91% across a variety of cancer diagnoses
tron; dopaminergic agents, such as amantadine, [76–80]. Therapies include (1) physical inter-
dextroamphetamine, bupropion, methylpheni- ventions such as yoga, acupuncture, massage,
date, and pemoline; adrenergic agents, such as and therapeutic touch, (2) mind–body methods
yohimbine and ephedrine; cholinergic agents, including relaxation techniques, music therapy,
such as bethanechol; and the selective phospho- and meditation, (3) dietary remedies such as
diesterase type 5 inhibitors. Numerous case herbs, homeopathy, specific diets, and vitamins,
reports and open-label studies examining SSRI- and (4) alternative medical systems including
induced anorgasmia report success in alleviating Chinese medicine and ayurveda, a traditional
reduced orgasmic function with some of these Indian medicine [59, 81]. Studies assessing the
agents. However, placebo-controlled studies efficacy of these treatments have found that there
generally have not shown differential effects are benefits to the patients regarding subjective
across these active treatments and placebo (for reports of relief of side effects  and increased
review, see Meston et al. [58]). coping ability [81], although the known effects
Hormone manipulation for the treatment of of alternative treatments on sexual difficulties
sexual dysfunction among cancer survivors has among cancer patients are limited (Table 11.2).

Table 11.2  Studies for the pharmacological treatment of orgasm dysfunction
References Design N Drugs Conclusion Level of evidence
Michelson Randomized, placebo- 57 women with fluoxetine- Amantadine (50, 100 mg), Improved orgasm with tx Daily diary and
(2000) controlled; 4 weeks induced sexual difficulty buspirone (20, 30 mg); and placebo; no difference clinician interview
fluoxetine continued during tx between tx vs. placebo
Modell Single-blind, placebo- 20 nondepressed women 3-week bupropion-SR (150 mg), Significant improvement of Sexual function
et al. [63] controlled; 12 weeks reporting nonphysiological 3-week bupropion-SR satisfaction with orgasm questionnaire
orgasmic difficulty (300 mg) intensity and overall sexual
satisfaction beyond placebo
Zajecka Cognitive behavioral 431 women; 65% reported Nefazodone (200–600 mg) Nonsignificant improvement in Sexual function
11  Disorders of Female Orgasm

et al. [64] analysis system of depression; 48% reported orgasm with psychotherapy, questionnaire,
psychotherapy, sexual dysfunction nefazodone, and combination physician-rated
nefazodone, or groups at 12 week compared depression severity
combined for 12 to baseline
Phosphodiesterase inhibitors
Caruso Double-blind, crossover; 51 premenopausal women with Sildenafil (25–50 mg) 25 and 50 mg sildenafil increased Sexual function
et al. [65] 12 weeks sexual arousal disorder orgasm frequency, compared questionnaire at
to placebo and baseline; placebo baseline and
increased orgasm relative monthly
to baseline
Basson Randomized, double- 34 oestrogenised postmeno- Sildenafil (50 mg) Reduced latency to orgasm for low Genital arousal
et al. [17] blind, placebo- pausal women with vaginal pulse amplitude (vaginal pulse
controlled; two acquired genital female responders only amplitude); orgasm
sessions sexual arousal disorder and latency (timed), and
impaired orgasm intensity (self-
Caruso Double-blind, crossover, 32 premenopausal women with Sildenafil (100 mg) Increased clitoral blood flow Sexual function
et al. [66] placebo-controlled; type I diabetes and seasonal and improved subjective sexual questionnaire
16 weeks affective disorder experience (arousal, orgasm,
sexual enjoyment, dyspareunia)
with sildenafil


Table 11.2  (continued)
References Design N Drugs Conclusion Level of evidence

Alternative treatments
Ito et al. [86] Double-blind placebo- 77 women, 6 with previous ArginMax herbal supplement 47% in ArginMax tx improved Sexual function
controlled; 4 weeks sexual dysfunction (ginseng, gingko, damiana, orgasm function at 4 weeks questionnaire
l-arginine) vs. 30% in placebo
Michelson Double-blind, 148 premenopausal women Mirtazapine (15–30 mg), No differences between tx Daily diary, sexual
et al. [87] randomized, parallel, with fluoxetine-induced yohimbine (5.4–10.8 mg), and placebo in diary function question-
placebo-controlled; sexual dysfunction olanzapine (2.5–5 mg) or self-report ratings of orgasm naire, structured
10 weeks function interview
Meston Cross-over, double-blind, 19 women with SSRI- Ephedrine (50 mg) Significant increase in orgasmic Sexual function
et al. [58] placebo-controlled; induced sexual dysfunction ability compared to baseline, questionnaire
8 weeks but not placebo
Meston Randomized, placebo- 167 sexually dysfunctional Gingko biloba extract (300 mg) Short-term use increased genital Genital arousal
et al. [68] controlled; 8 weeks women arousal response; long-term (vaginal pulse
sex therapy alone increased amplitude), clinical
orgasm function interview, sexual
Hormonal treatments
Krychman Open-label; case series 3 women with history Testosterone, varied Sexual satisfaction and desire Comprehensive
et al. [84] of breast cancer administration improved for two of three sexual medicine
women evaluation
Y.P. Khouri et al.

11  Disorders of Female Orgasm 159

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lighting the prevalence of orgasm dysfunction
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Psychosomatics. 1989;30:166–73.
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this group, physicians must broaden their focus der and in women with hypoactive sexual desire dis-
order. J Sex Marital Ther. 2003;29:39–46.
to all elements of their patients’ well-being,
16. Rosen RT, Taylor JF, Leiblum SR, Bachmann GA.
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Chapter 12
Sexual Pain Disorders

Corrie Goldfinger and Caroline F. Pukall

Keywords  Adjuvant treatment • Anodyspareunia treatment strategies. The lack of knowledge
• Anxiety/fear • Biofeedback • Chemotherapy surrounding this multifaceted condition only
• Cognitive-behavioral therapy • DSM • serves to increase the difficulty inherent in its
Dyspareunia • Hormones • Hysterectomy • assessment and management.
Injectable therapy • Menopause • Oopherectomy This chapter focuses on conditions that cause
• Pain • Pelvic floor muscles • Physical therapy dyspareunia in women and attempts to conceptu-
• Topical therapy • Tricyclic antidepressants alize them within a biopsychosocial framework.
• Vaginal atrophy • Vaginal dilation • Vaginismus The majority of the chapter covers pain condi-
• Vestibulectomy • Vulvodynia tions considered to be idiopathic (i.e., with no
known physical cause); however, organic pain
conditions (i.e., those due to medical conditions)
Introduction are also summarized. Sexual pain disorders in
men are briefly outlined, and the chapter con-
cludes with a discussion of sexual pain experi-
Sexual pain disorders encompass a broad array enced by patients with cancer.
of conditions which lead to difficult or painful
sexual intercourse. The term dyspareunia is
used in this chapter to describe recurrent or
persistent urogenital pain that interferes with
Classification of Sexual
sexual and/or nonsexual activities. Prevalence
estimates of dyspareunia ranged from 0.4 to Pain Disorders
61% in one recent systematic review [1], and
there is considerable evidence to suggest that Two main challenges in reviewing the sexual pain
these varying rates reflect the inconsistency of disorders are: (1) the varying methods of classifi-
dyspareunia definitions as well as differences in cation and definitions by medical and psychiatric
study design and measurement [1–3]. Women bodies, as well as various authors, and (2) the cur-
with dyspareunia, in general, suffer negative rent discrepancy between the classification sys-
impacts in psychosocial and sexual areas of tems and empirical findings. The DSM-IV-TR [5]
their lives [4]. Despite the common clinical definition of sexual pain disorders within the sex-
complaint of dyspareunia, there is still limited ual dysfunction category includes dyspareunia and
knowledge regarding its etiology and effective vaginismus not solely due to medical conditions,
while their organic counterparts are coded as sex-
ual dysfunctions due to a general medical condi-
tion. Dyspareunia is defined as “recurrent or
C. Goldfinger (*)
Department of Psychology, Queen’s University, persistent genital pain associated with sexual inter-
Kingston, ON, Canada course,” (p 556) while vaginismus is “recurrent or

J.P. Mulhall et al. (eds.), Cancer and Sexual Health, Current Clinical Urology, 163
DOI 10.1007/978-1-60761-916-1_12, © Springer Science+Business Media, LLC 2011

164 C. Goldfinger and C.F. Pukall

persistent involuntary spasm of the musculature of investigating the causes of the pain and to more
the outer third of the vagina that interferes with appropriate treatment modalities.
intercourse” (p 558). Diagnostic criteria also Another classification system is that of the
require that pain specifiers be placed on the cause International Society for the Study of Vulvovaginal
of the pain (due to psychological factors, or due to Disease (ISSVD). This system is specific to vul-
combined psychological and medical factors), and var pain conditions and is in line with viewing
whether the condition is lifelong or acquired and dyspareunia as a pain, rather than a sexual, disor-
global or situational. der. This classification system (summarized in
As will be discussed in further detail later, there Table 12.1) organizes vulvar pain into two cate-
are a number of concerns related to the definition gories: (1) those related to a specific disorder, and
of vaginismus given findings from empirical stud- (2) vulvodynia. Vulvodynia is defined as “vulvar
ies. Additionally, the DSM-IV-TR makes a clear discomfort, most often described as burning pain,
distinction between organic and idiopathic pain. occurring in the absence of relevant visible find-
Pukall et al. [6] have argued, however, that there is ings or a specific, clinically identifiable neuro-
neither empirical nor theoretical support for this logic disorder” [11] (p 775). Vulvodynia is further
distinction. They further purport that this distinc- classified into subtypes depending on (1) the
tion may lead health professionals to assume a psy- location of the pain [i.e., localized (pain in a par-
chogenic cause of the pain if no medical cause can ticular vulvar area) versus generalized (pain
be found, which can often result in the woman affecting the whole vulvar region)], and (2) the
being told that the pain is “all in her head,” leading temporal characteristics of the pain [i.e., pro-
to a referral to a psychiatrist or other mental health voked (pain that only occurs when elicited by
professional. Furthermore, by classifying dyspare- some form of pressure), unprovoked (pain that
unia as a sexual dysfunction, the attention is placed exists on a constant basis and needs no provoca-
on sexual aspects of the disorder, rather than on the tion), or mixed (a combination of provoked and
major clinical symptom of the disorder, pain. This unprovoked pain)]. The criteria also stipulate that
classification is therefore being challenged by a provoked pain can be elicited in sexual and/or
body of evidence that supports the conceptualiza- nonsexual situations. Although this system does
tion of dyspareunia as a pain disorder that inter- not take into account all forms of dyspareunia
feres with sexual function rather than as a sexual (e.g., deep pelvic pain), it provides a model to
dysfunction per se [7–9]. Classifying dyspareunia classify sexual pain disorders such that the focus
as a pain disorder may lead to different ways of is on the primary presenting symptom of pain.

Table 12.1  Classification of female vulvar pain disorders and male sexual pain disorders
Classification of vulvar pain Classification of sexual pain disorders in men
Type 1: Vulvar pain related to a specific disorder Type 1: Isolated ejaculatory pain (pain during or after
(a)  Infectious (e.g., candidiasis) ejaculation)
(b)  Inflammatory (e.g., lichen planus) (a)  Identifiable cause
(c)  Neoplastic (e.g., squamous cell carcinoma) (b)  Idiopathic
(d)  Neurologic (e.g., herpes neuralgia) Type 2: Pain associated with sexual activity, as part of
Type 2: Vulvodynia chronic pelvic pain syndrome (CPPS)
(a)  Generalized Type 3: Painful genital conditions (e.g., chronic testicular
(i)  Provoked pain) which interfere with sexual activity or are
(ii)  Unprovoked associated with sexual dysfunction
(iii)  Mixed Type 4: Other causes of sexual pain
(b)  Localized (a)  Penile causes (e.g., phimosis)
(i)  Provoked (b) Other types of sexual pain disorder
(e.g., anodyspareunia)
(ii)  Unprovoked
(iii)  Mixed
Adapted from Luzzi and Law [10] and Moyal-Barracco and Lynch [11]

12  Sexual Pain Disorders 165

Sexual Pain Disorders information obtained during the interview but may
include the following: visual examination of the
vulva, preferably with the use of vulvoscopy; sen-
Pain Related to a Specific Disorder sory exam using a cotton swab (see Section
“Assessment” under “Vulvodynia” below for fur-
Table 12.2 summarizes a variety of conditions that ther details); speculum exam of the vagina; manual
can cause recurrent or persistent dyspareunia in exam with one finger to assess the urethra, blad-
women. As evidenced by this extensive, yet likely der, and pelvic floor muscles (PFMs); bimanual
nonexhaustive, compilation of conditions, it is exam to assess the uterus and adnexa; and a recto-
important that a thorough medical history inter- vaginal exam. A number of tests may also be con-
view and physical exam be conducted to rule out ducted based on the physical exams and could
physical illness or abnormalities as the cause of include: wet mount and cultures of vaginal dis-
the pain. Goldstein [13] delineates the broad array charge, vulvar or vaginal biopsy, serum testing,
of issues that should be addressed in the medical medical imaging, diagnostic laparoscopy, cystos-
history interview and encourages that the health copy, or colonoscopy. Although it is important to
professional obtaining the history be sensitive to rule out specific medical causes for sexual pain in
the woman’s concerns, validate her emotional women, due to the painful nature of these women’s
responses to her pain, and allow the woman to tell concerns, exams and tests should only be per-
her story while guiding them through the process formed when there is sufficient reason to believe
to get as much detailed information as is required. that their outcome will be helpful in determining a
The areas covered in the medical history interview diagnosis.
for women presenting with sexual pain include:
past and current urogynecological functioning and
concerns, urogenital and other pain history, void-
ing habits, dermatological concerns, sexual func- Vulvodynia
tioning, and mental health. The ISSVD website
( has an extensive questionnaire The two main subtypes of vulvodynia are pro-
that women can fill out before seeing their doctor. voked vestibulodynia (PVD; previously called
The physical exams conducted will depend on the vulvar vestibulitis syndrome), characterized as

Table 12.2  Causes of dyspareunia
Disorders of the urinary
Disorders of the vulva Vaginal disorders Disorders of the pelvic area and gastrointestinal tract
Infections (bacterial, viral, Congenital factors Hysterectomy Acute and chronic cystitis
fungal) (vaginal agenesis, Adenomyosis of uterus Interstitial cystitis
Irritation (mechanical, duplication, Ovarian pathology Urethral lesions
chemical) septation) Prolapsed adnexa Urethral diverticulum
Dermatoses Structural abnormali Leiomyoma or benign Urethritis
Vulvar papillomatosis ties from surgery tumors of the uterus Fistulas
Hymenal stenosis or radiation Salpingitis Inflammatory bowel
Adhesions Pelvic organ prolapse Pelvic inflammatory disease disease
Trauma (cystocele,
Endometriosis Diverticulitis
Episiotomy scars Pelvic adhesions Hemorrhoids
Decreased lubrication Pelvic floor muscle Crohn’s disease
Atrophic vaginitis
Peri/postmenopausal or dysfunction
lactation atrophy Pelvic venous congestion
Estrogen deficiency Neuropathies (nerve
Inflammatory or
Inflammatory or allergic entrapment)
allergic reaction
Cancer (radiation)
Adapted from Glazer [12]

166 C. Goldfinger and C.F. Pukall

localized and provoked pain of the vulvar or penetration), while fewer (3.3%) described pain
­vestibule, and generalized vulvodynia (GVD), consistent with GVD (i.e., chronic burning or
characterized as generalized and unprovoked knife-like pain). The authors found that although
pain. There is some controversy, however, over the prevalence of PVD-like symptoms decreased
the distinction between the various subtypes of with age, GVD-like symptoms maintained the
vulvodynia based on location and temporal pat- same prevalence across age groups. Furthermore,
tern because many women have pain that is both although Caucasian and African-American women
localized and generalized [14, 15]. had similar prevalence rates, Hispanic women were
PVD is the most common form of vulvodynia. 80% more likely to have chronic vulvar pain [18].
It is typically described as a sharp or burning pain
at the entrance of the vagina in response to con-
tact or pressure to the vulvar vestibule. Friedrich Etiology
[16] outlined the three diagnostic criteria for
PVD: (1) severe pain upon vestibular touch or Research into the etiology of vulvodynia has been
attempted vaginal entry, (2) tenderness to pres- varied and sometimes inconsistent, leading to the
sure localized within the vulvar vestibule, and (3) conclusion that there are likely multiple etiologi-
physical findings limited to vestibular erythema cal pathways for and numerous maintaining fac-
(i.e., redness) of various degrees. Only the first tors of the pain. Table 12.3 summarizes research
two criteria have shown to be diagnostically valid findings supporting various etiological theories
and reliable [17]. The onset of pain may be at first for PVD. Several studies investigating vestibular
intercourse attempt (i.e., primary PVD) or may
develop after some period of pain-free intercourse Table 12.3  Etiological theories of provoked vestibulodynia
(i.e., secondary PVD). Alternatively, women with Vestibular tissue factors
GVD describe chronic vulvar discomfort that is Increased inflammatory mediators [19]
not dependent on contact, characterized by a Increased nerve fiber innervation [19–22]
Increased subepithelial heparanase activity [23]
burning or stinging sensation covering the entire
More pain receptors [24]
vulvar region (e.g., labia minor and majora, Increased blood flow [25]
perineum). Some women with GVD may also Increased pain-related peptides [26]
meet the diagnostic criteria for PVD. Central nervous system dysfunction
A diagnosis of vulvodynia is a diagnosis of Increased sensitivity to vestibular touch [27–30]
exclusion, i.e., specific causes for the pain must Increased sensitivity to touch in nonvestibular areas
be ruled out. It is based on the woman’s self- [30, 31]
report of vulvar pain (i.e., pain location, quality, More pain related complaints [30, 32, 33]
and description), and in the case of PVD, the Increased neural response to vestibular touch and pain [34]
More grey matter in pain-related brain areas [35]
diagnosis is also dependent on the presence of
Genetic factors
pain during the cotton swab test (the standard
Higher incidence of alleles associated with abnormal
gynecological method for diagnosing PVD [16]). regulation of inflammation [36–38]
Higher incidence of alleles associated with immune
defence against micro-organisms [36]
Epidemiology Hormonal factors
Higher risk of PVD in oral contraceptive users [39–41]
A population-based study estimated the preva- Higher risk of PVD in those with early menarche and
painful menstruation [39, 42]
lence of vulvodynia in an ethnically diverse sam-
Decrease in estrogen receptor expression [43]
ple of almost 5,000 women between the ages of Oral contraceptive pills changes in hormonal reception
18 and 64 in the United States [18] and found a and morphology of vestibule [44, 45]
lifetime prevalence rate of 15.6% for chronic vul- Pelvic floor muscle dysfunction
var pain. A majority of these women (12.4%) Increased pelvic floor muscle tone [46–48]
reported a pain pattern consistent with PVD (i.e., Pelvic floor muscle instability, poor contractile
excessive pain on contact with attempted insertion strength, and poor recovery after contraction [49]

vulvar injury) and may not have the ability to terminate this response. factors are findings of a higher incidence of including hypertonicity and instability of the several alleles in women with PVD. Interestingly. associated with PFM dysfunction. pointing toward changes in cutaneous perception trolled quantitative sensory testing (QST) and as a cause for the pain [52]. due to the correlational by a micro-organism that may cause symptoms design of the studies. PFM dysfunction. sexual. The authors posit that the tension acts Moreover. infection. Given the multitude of etiological theories for sis for this contribution is that women with PVD both PVD and GVD. GVD demonstrated [27. 34]. including depression and state tone) of the PFMs in women with PVD suggests and trait anxiety.’s [48] study on hypertonicity (i. Evidence from con.. in pain-related cognitions. psychosocial and sexual of PVD [36]. One hypothe. the increased has been conceptualized as a neuropathic pain sensitivity exhibited by women with PVD is not condition for some time. Numerous studies have as electromyographic biofeedback [46]. Further support to this theory are the tion of findings supports a general view of PVD findings that women with GVD are more likely as a neuropathic pain condition. with early research restricted to the vestibule. to have other CRPSs such as interstitial cystitis Further implicating the role of systemic [55. PVD. It has been proposed pared to PVD. 30]. scarcer and less clearly conceptualized as com- cessing plays a role in PVD. findings suggesting possible complex regional tion to a peripheral.e.. it has been suggested that who present with some of these alleles may be either subtype of vulvodynia may be caused by at increased risk for an inflammatory immune more than one factor and that the contributing response following some trigger (e. Similar to PVD. yeast factors likely differ for each woman [58]. 56]. The onset of GVD commonly that these vestibular factors could lead to a height. supporting muscles. which has been previously cream application or laser surgery [51]. rather than compared to nonaffected women [4.g. lead to increased sensitivity of the vestibule in Knowledge of these issues helps to better under- affected women [44]. Numerous psychological. increased logical distress. causes. This theory is Research has shown that vulvodynia is asso- based on the findings of PFM dysfunction in ciated with negative impacts such as reduced women with PVD as well as improvements in quality of life. follows some acute event. are more com­ is that alterations in the hormonal milieu may monly conceptualized as consequences of pain. with highly reported ened sensitivity in response to pressure applied to triggers being local treatments such as vulvar the vestibular tissue. including greater . The pro- longed inflammation may trigger other changes Psychosocial Factors and lead to an increased sensitivity both within and outside the vestibule [37. 60–63]. stand the experiences of affected women and may It has also been suggested that PVD may be guide treatment planning.12  Sexual Pain Disorders 167 tissue differences between women with PVD and Research into the etiology of GVD has been nonaffected women support that altered pain pro. pain modulatory dysfunction pain syndrome (CRPS) or pudendal neuralgia in women with PVD [28–30. [53. however. 54]. Alternatively. affected women show differences as a maintaining and exacerbating factor in PVD. in addi. although the exact attributed as causes nor as resulting from the causal mechanism is not clear. and relational the presence of some alleles might increase factors have been investigated in women with susceptibility to a lower genital tract infection vulvodynia. however. in women with vulvodynia as that hypertonicity likely results from. These factors. a possible genetic contribution. One possibility pain. This combina. Reissing also found significantly higher levels of psycho- et al. and more recent brain imaging studies supports a central. factors associated with vulvodynia can neither be monal contribution to PVD. 50]. has been implicated in GVD [57]. Other findings support a hor. including feeling out of control of PVD symptoms following PFM treatments such one’s life and body [59].

many women reduce the frequency of or completely stop sexual activity due to pain [59]. and lower sexual satisfaction scores [61.g. a tool that exerts motion (see Fig. Although it vulvodynia takes a multidisciplinary approach would be intuitive to assume poorer relationship where possible [74]. it may not be reliable for research vulvodynia. ical utility. and more likely to participate in partnered sexual activity despite the lack of desire to do so [61. It has been recommended that the assessment of ing the onset of their vulvar pain [69]. 77] therefore some time. pain sensitivity as a result of treatment.1  The vicious cycle of pain less likely to make sexual advances. logical test for diagnosing PVD [16]. measurement error due to inconsis- chological. given the intimate connection between vaginal penetra- tion and the experience of pain.1) in which psychological fac. ratings upon palpation. a formal evaluation of the PFMs by a pelvic increases in pain and distress. In addition to psychological impacts. Pukall and colleagues [76..g.168 C. affected and non­affected women [4. 71. Pukall degrees of hypervigilance and catastrophizing [30. This assessment would functioning among women with vulvodynia. tency of pressure application is inherent in the test mental to understanding and treating women with and. Assessment Women also report negative impacts on self- esteem. the include a mental health professional to conduct empirical findings in this area are mixed. decreased desire and ting. . Not surprisingly. a vicious cycle of pain is put into developed the vulvalgesiometer. Studies examining women with vulvodynia and those comparing affected and nonaffected women demonstrate negative effects on sexual desire and arousal. 64. catastrophizing). 68–70]. 65]. the only vulvodynia diagnostic assess- others finding poorer relationship functioning and ment is the cotton swab test. The test This pattern of findings suggests that vulvo. relief if the muscle dysfunction is not addressed. and a gynecologist and some studies finding no differences between physical therapist to conduct the physical exams. Once vulvar pain has been present for use. women with vulvodynia are Fig. Goldfinger and C.. Although it has good clin- This perspective emphasizes that biological. poorer vaginal lubrication. sexual and pressure pain thresholds in a clinical research set- relationship difficulties (e.F. 12. The continuous floor physical therapist is recommended for treat- interaction of all of these factors explains pain ment planning because some treatment options maintenance and possible exacerbation despite the may be less likely to result in complete pain absence of physical findings for the pain. Furthermore. standardized pressure to the vulva to measure tors (e. with the clinical interview. and pelvic floor muscle dysfunction (e. self-confidence. Given the hypertonicity. anxiety. and social factors are seen as funda. 66–70].. therefore. and Thus far. 72]. more likely to refuse a partner’s sexual advances. and it supports conceptualizing sitization [75] while recording the woman’s pain vulvodynia from a biopsychosocial viewpoint.g. 12. heightened reactivity) – which role that PFM functioning plays in both PVD and initially result from the pain – lead to further GVD. consists of palpating vulvar sites with a cotton dynia has a widespread negative impact on affected swab in a randomized fashion to control for sen- women’s lives. 73]. psy. vulvodynia also has consequences on sexual functioning. the standard gyneco- satisfaction among affected women [70. and body image follow. and can be useful in detecting differences in arousal). lower sexual self-concept. lower intercourse and orgasmic frequency.

teroid and lidocaine have the most promising lubrication) outcomes in nonsurgical medical options. and treatment history options have received empirical support from and outcomes. unprovoked A recent review of various treatment options vs. The interview should provide the clinician with extensive information about the woman’s history of pain (often best obtained through the natural Treatment history approach) as well as her current reasons for seeking treatment. PFM therapies. leading to difficulties in assessing the behavioral) outcome of the intervention under study.. pain mediators and the There are numerous treatment recommendations impact that pain has on various aspects of her for both PVD and GVD.12  Sexual Pain Disorders 169 Other than the physical exams and tests used relationship adjustment may prove useful to clini- to rule out specific causes for sexual pain (see cians in obtaining more detailed information Section “Pain Related to a Specific Disorder” from the affected woman. the studies investigating medi- treatments cal treatment options had numerous method- Perception of pelvic floor muscle tension ological limitations including the lack of control/ Medical history comparison group(s). mixed) for PVD found success rates for medical treat- Factors that trigger or exacerbate pain Factors that reduce pain ments – including topical.g.. injectable. Treatment options can be categorized sexual and psychological functioning. In addition. and as: topical. ings. lidocaine 5% applied Past sexual functioning daily and combined injections of both corticos- Impact of pain on sexual functioning (e. arousal. comorbid disorders. many are based on expert opinion and are intensity) yet to be empirically proven. (RTCs). the surgery group had the highest . random assignment. vulvodynia. however. cognitive. psychological. The Impact of pain on mental health/well-being authors of the review study conclude that. Sexual satisfaction This same review also investigated the extant Past and current sexual practices History of abuse literature investigating the effectiveness of surgical Relationship quality and interpersonal functioning treatment options for PVD. antecedents) Duration of pain PVD and/or GVD. Temporal pattern of pain (provoked vs.4 summa- above). and follow-up. Although some of these Location of pain recommendations are based on empirical find- Perception of pain characteristics (e. or alternative. In general. The use of standardized self. however. Table  12. controlled studies or randomized controlled trials administered questionnaires to measure pain. the clinical interview is the most impor.5 summarizes Pain the various treatment options recommended for Onset of pain (when did it start.4  Clinical interview components for vulvodynia mended to these patients. some studies Comorbid disorders Food and medication intake did not control for participants receiving addi- tional treatments between the intervention and Psychological functioning Responses to pain (emotional. In one randomized Impact of pain on relationship functioning trial. surgical. yielding success rates Partner’s sexual or genital symptoms ranging from 61 to 94% [117]. rizes the information that should be obtained tant assessment tool with respect to diagnosing during the clinical interview. Table 12. and definition of Dermatological concerns and allergies therapeutic success. Additionally. Urogynecological functioning and concerns blinded treatment evaluation. as well as in treatment planning. lifestyle changes are often recom- Table 12. few treatment life. given Sexual and relationship history and functioning the research conducted.g. injectable. systemic. quality. and sys- Previous diagnoses and tests/assessments temic medications – ranging from 13 to 67% Past treatments attempted and outcomes of those [117].

. lidocaine) (PVDc. these findings are based on small There have also been a number of empirical uncontrolled studies. although this procedure recent study investigated individual cognitive- has shown to have the highest success rates of any behavioral therapy (CBT) in women with various treatment for PVD. it is not effective for all women forms of vulvodynia. GVDa) Nitroglycerin (PVD. such as . although the importance of treating the psy- support for tricyclic antidepressants [95].. GVD) Capsaicin (PVD) Physical therapy (PVDa. nortrip. 47. methylpredniso. desipramine) (PVDc. In general. 99–102] Vestibulectomy: (1) local excision. 79. Use of mild soap and not applying soap to the vulva tyline. with all forms of vulvar pain is emphasized [118]. 57. GVD) Gabapentin (PVD. GVDb) Lifestyle changes to reduce irritation in PVD and GVD Botulinum toxin type A (PVD. cognitive-behavioral. The effectiveness of group CBT treatment outcome research for women with in women with GVD has not yet been empirically GVD. the PFMs in women with vulvodynia. These Cognitive-behavioral interventions for vulvo. GVD) Steroids (PVDa. in addition. 102]. (3) perineoplasty (PVDa. chosexual and relationship functioning in women entin [94]. Pukall Table 12. a small percentage of reported in three studies in which sex therapy and participants who underwent this relatively invasive pain management were combined in a group for- procedure reported worse outcomes following the mat for women with PVD [99. betamethasone.. 101. biofeedback [46. and botulinum toxin type A [93]. Surgery is not generally investigations of the use of treatments targeting recommended for women with GVD. compared to women who received supportive psy- There is considerably less medically related chotherapy [100]. GVDa) Alternative therapies [112–116] Injectable therapies [88–93] Acupuncture (PVD) Corticosteroids (e. amitriptyline.g. (2) total vestibulec. GVD) Electrical stimulation (PVD. studies have provided evidence for the effective- dynia include pain management and sex therapy to ness of surface electromyographic (sEMG) target pain reduction and sexual functioning.g.. ­Cognitive-behavioral therapy (group tomy. GVDb) or individual format) (PVDb. One treatment [78]. 104. GVD) Cotton underwear Oral medication [94–97] Avoid fabric detergent and softeners on underwear Tricyclic antidepressants (e. GVDa) Electromyographic biofeedback (PVD. 78.g. 108] as well as other Success rates ranging from 43 to 86% have been single physical therapy modalities. Therefore. 103–111] Anesthetics (e. GVD) Hypocontact vulvar therapy (PVD) Estrogens (PVDa. however. Hypnotherapy (PVD) lone) (PVDa. GVDb) Laser therapy (PVD) Interferon (PVDb.F. gabap. gabapentin) (PVDa. there is some limited empirical tested.5  Treatment options for vulvodynia Behavioral.g. GVDc) Lubrication (without propylene glycol) during sexual Other therapies [98] activity Local anesthetic nerve blockade (PVD) Note: Superscript letters refer to the percentage of clinicians who reported recommending the therapy for PVD or GVD based on Updike and Wiesenfeld’s [123] survey a 25–49% b 0–24% c 50–74% d 75–100% drop-out rate. and alternative Medical/surgical treatment options treatment options Surgery [78–83] Psychological therapies [78. GVDa) Topical therapies [84–87] Pelvic floor therapies [46. GVDa) Vaginal dilation (PVD.170 C. 79. and found significantly and some women may choose to not undergo the greater improvements in pain and sexual outcomes procedure due to its invasiveness. GVDd) Unscented and dye-free cotton menstrual pads Anticonvulsants (e. Goldfinger and C.

and sEMG biofeedback in the The algorithm may be helpful for some health treatment of PVD [78. low oxalate diet women with PVD. and they only included nonmedical treatment modalities (physical and psychosocial therapies) [121. 111]. and 35%. ment options does not provide adequate results. and 16% of clinicians. strength and desensitizing local tissues in women In 2005. they did not include any control Women groups or standardized treatment protocols. one Dyspareunia is a commonly reported problem of a woman presenting with PVD and another by postmenopausal women. should not be recommended as a tibulectomy. how. 35. family physi. Some physical therapists.12  Sexual Pain Disorders 171 electrical stimulation [110] and vaginal dilation they would use for the cases [123]. Both pain and psychosexual treatment that has proven effective for all women. dyspareunia ranging between 2 and 29% among gynecologists. and laser therapy [114] is prelimi. cal therapy) in women with PVD. A recent survey including two scenarios. and psychosexual functioning [103. such as bio. Success rates for the care professionals as it offers a step-by-step three groups were 68. it is important that women with vulvodynia Despite the importance placed on multidisci. and this pattern was maintained when com. 126].and long-term effectiveness of vestibulec. [124] outlined a treat- with PFM dysfunction [120]. purport that certain therapies. commonly reported treatments for PVD were tri- ever. 79]. outcomes in all the three groups were maintained therefore. The most commonly reported treat- of the PFMs (typically termed pelvic floor physi. however. was sent to American clinicians found point prevalence rates of postmenopausal known to treat women with vulvar pain (e. however. Two studies line therapy by 27. 11.. These treatments were used as first solitary treatment modality [119]. 116]. approach to treatment. Supporting a case-by-case paring vestibulectomy to biofeedback at 6 months treatment plan is the fact that there is no single posttreatment [78]. local anesthesia. 106]. nary and has shown some success in treating biofeedback/physical therapy. 109. ment algorithm for vulvodynia with the recom- Research on alternative treatment strategies mendation that treatment should follow the including acupuncture [112. and 3% of clinicians. Surgery is recommended conducted to date has been a RCT comparing the only in the case that this progression of treat- short. with these found evidence of improvements in both pain treatments being used as first line therapy by 55. Haefner et al. only tions as successful treatment may take time and two published studies have assessed the effective. The most [107. these studies gabapentin. Results from this Regarding GVD. 115].g. [127] with GVD. develop realistic treatment goals and expecta- plinary treatment approaches for vulvodynia. there is no empirical study indicated a broad array of variability in the support for pelvic floor physical therapy despite treatment of vulvodynia across clinicians and its effectiveness in normalizing and facilitating support the need for more rigorous and con- normal muscle tone and in increasing PFM trolled studies to aid in treatment planning. with calcium citrate supplementation. and ves- feedback. hypnotherapy following progression: vulvar care measures. ness of multimodal treatment programs for PVD. Furthermore. population-based studies and much higher rates cians) and asked them to identify what treatments among clinical samples (11–45%). a number of Vestibulectomy resulted in significantly lower pain authors support a more individualized treatment levels than the two other treatments at posttreat. have provided support for multimodal treatment respectively. Dyspareunia in Postmenopausal itive outcomes. injections. dermatologists. oral medications. tomy. cyclic antidepressants. As compared . topical medications. Although both studies resulted in pos. and physical therapy. a complete “cure” may not be achievable. exams [125. approach based on the interview and physical ment. ments for GVD were tricyclic antidepressants. 39. at a two and a half year follow-up [79]. 122]. prognosis is never clear. group CBT. and CBT The most extensive treatment outcome study with sexual counseling. [113. Kao et  al. respectively.

and methodological limitations of research in this area [127].. [6] exams. IA) be offered to those women cascade of events following declining levels of who wish to avoid HRT [139]. Another major concern related to the clas- therefore point out the importance of assessing sification and definition of vaginismus is the role for possible nonbiomedical factors that may play of pain. and shortening [131. relationship ference that the condition has on nonsexual activi- difficulties. Although there endogenously produced estrogens. and physi- changes in the vagina. It both researchers and clinicians.F.g. Kao et  al. of vaginismus. cal therapy have also been recommended as These changes can result in vulvovaginal and treatment avenues in postmenopausal women urogenital atrophy. negative attitudes cognitive components.172 C. 142] and are therefore not unique to for postmenopausal dyspareunia [139]. pareunia has consistently been attributed to the Cedar Rapids. In line with the narrowing. hormone replacement therapy (HRT) symptom of dyspareunia (e. couples therapy.. As with Several authors have pointed to the impor. current definition is that there is no empirical These findings suggest that factors other than basis for including vaginal spasm as a diagnostic hormone-related changes may be involved in the criterion given that muscle spasms are neither development of postmenopausal dyspareunia. such as Replens® (Lil’ Drug Store Products. the classification of vaginismus as a tance of psychosocial factors in contributing to sexual pain disorder and the wording of its defini- or maintaining sexual dysfunction in postmeno.g. poor body image. and loss ties such as tampon insertion and gynecological of social support [133. There are currently mixed findings with There are also a number of researchers who respect to the effectiveness of various hormonal purport that dyspareunia and vaginismus cannot regimes in treating postmenopausal dyspareunia be differentiated from one another given that: (1) with concurrent vaginal atrophy [135–138]. inclusion of nonhormonal treatments for this One recently published literature review population. and (2) the PFM dys- from a randomized. 132]. The main argument against its presence of dyspareunia and vaginal atrophy. and disregard the inter- towards postreproductive sexuality. ings its definition and its classification as a sexual denced a significant relationship between the pain disorder. and cytological and chemical tiveness. 144]. and cytological evaluations. vaginal dryness [128–130]. Findings vaginismus [143. sex therapy. vaginal penetration problems often present as a however. exclusive nor specific to vaginismus [47]. These events are no empirical studies evaluating their effec- include tissue aging. Goldfinger and C. 134]. open-label study resulted in a function that interferes with penetration is a . urethra. mainly surround- also concluded that not one single study evi. Pain is not currently a diagnostic criterion a role in postmenopausal dyspareunia in addition in the DSM-IV-TR and no information is provided to the physical exam. This review critically examined the five extant studies investigating the relation- ship between postmenopausal dyspareunia and Vaginismus either estrogen levels or vaginal atrophy and found inconsistent relationships between the Vaginismus has received much criticism from presence of dyspareunia and estrogen levels. the collection of hormonal on the pain characteristics (e. with dyspareunia [131. location. and bladder. Pukall et  al. dyspareunia. postmenopausal dys. partner sexual dysfunction. quality) assays. 140]. tion focus on the sexual nature of the condition to pausal women including negative perceptions of the exclusion of its more central behavioral and menopause. in women with is currently considered the primary intervention PVD) [141. [127] encourage the investigating dyspareunia in postmenopausal empirical study of the role of psychosocial women offers novel insight into the theoretical factors in these women. Pukall to the multiple etiological theories for vulvodynia recommendation that nonhormonal moisturizers in premenopausal women.

2). combined include vaginismus as a result of PVD [141– physical therapy modalities and cognitive-behavior 143]. accurate prevalence rates do not exist. including catastrophizing and fear of pain with only 14% of women being able to have or penetration. As with vulvodynia. Adapted from Reissing [153] [147] (p 226). A recent review out vaginismus [151. despite the woman’s expressed wish to do so. affected niques are often accompanied by education to women demonstrate strong emotional and behav. ness of the standard treatment for vaginismus iety. 152]. A number of etiological theories exist for vaginismus. The standard treatment The latter theory is supported by findings that for vaginismus. in working toward penetration. A consensus committee has recommended the following revised definition of vaginismus: “persistent difficulties to allow vaginal entry of a penis. Given the problems with the defi- nition. There is variable involuntary pelvic muscle contraction. not found in the few controlled trials that exist ful experience – or even a negative expectation [159]. however. (phobic) avoidance and anticipation/ fear/experience of pain. 126]. improve sexual knowledge and attitudes. negative expectations of penetration [153]. such as fear of pain or poor body image.  12. sexual abuse prevalence and understanding as well as sensate focus to aid rates are not higher in women with versus with. Structural or other phys- ical abnormalities must be ruled out/addressed” Fig. . These tech- vaginal penetration [150]. the same encouraging results are Fig. therapy [155]. with 90% of likely painful event leads to confirm the woman’s women being able to achieve penetration [161]. and therefore the assessment. includes vaginal dila- fear of pain is the primary reason that women tion combined with progressive desensitization with vaginismus report for their avoidance of and relaxation techniques [153]. in addition. increased tone. These negative cognitions result penetration at completion of the treatment [160].. and Although initially thought to play a role in the couple intervention to improve communication etiology of vaginismus.2  The vicious cycle of vaginismus. exposure to reduce fear and avoidance. rates range from 12 to 17% [145. A recent RCT resulted in modest effective- about penetration – leading to symptoms of anx. 12. negative sexual attitudes [156]. and a specific penetration phobia. surgery to widen the introitus poorer strength) [47]. however. in clinical settings. Some of the proposed theories including anxiolytic medication [154]. botulinum toxin injections [157]. which in study on the effectiveness of therapist-aided turn.e. psycho- ioral reactions to attempted penetration and therapy to reduce related psychological issues engage in active avoidance of penetration [47]. much ened tone during an attempt. with either an initial negative or pain. 146]. the experience of vaginismus although uncontrolled studies indicate very posi- has been proposed to act cyclically (see tive outcomes. and topical [148–150]. of vaginis- mus. researchers support an indi- Treatment outcome studies for vaginismus vidualized treatment approach for women with have investigated various treatment options vaginismus [126]. in a woman either avoiding penetration or being When the same researchers conducted another hypervigilant to pain during attempts. PFM dysfunction (i.12  Sexual Pain Disorders 173 symptom in almost all women with vulvovaginal pain [48. of vaginismus treatment studies concluded that Like dyspareunia. anesthetic creams [158]. and/or any object. This failed and higher success rates were found. leads to pelvic floor reactivity and height. a finger.

2 to itself. diagnostic imaging) to rule out side effects of cancer treatments. Although breast cancer and its sex with men (MSM) and has been found to surgical treatment do not cause dyspareunia. prevalence rates were 12 [169] and 14% [170] in two studies of MSM. Goldfinger and C. They also outline unia should be added to future revisions of the specific causes of ejaculatory pain which have DSM under the sexual pain disorders category. nonetheless. ovarian. This pain ducted among women treated for breast or gyne- experience has been studied in men who have cological cancers. In and classification system for sexual pain disor- addition to factors such as penis size. survivors. and the pelvis (e. however. Management of idiopathic pain conditions follows the recommended approach to CPPS and include symptom assess- ment and control. deep breathing. cancers that affect rate of CPPS is approximately 2–3% [166]. and other pelvic causes (e.g. There is much less research available with the pain during anal intercourse was reported to respect to pain associated with sexual activity in cause significant distress and/or interpersonal dif- men. this system distinguishes between organic and idiopathic pain. For instance. The majority of research in the area of sexual sistent pain experienced by the receptive partner side effects of cancer treatment has been con- during anal intercourse” [169] (p 289).g. with factors such as duration of pain and psychological issues related to diagnosis. colorectal cancer) and sexual one study of men with CPPS indicated that 24% organs (e. Also similar to sex- Sexual dysfunction in cancer survivors. includ- ual pain in women. mercury poisoning. abdominal. cancers in women. and various medical tests (e. lack of ders in men (summarized in Table  12. and Assessment strategies with men follow similar prostate cancers in men) can all lead to dyspare- steps to that of women and include a thorough unia even before diagnosis or treatment.g. chronic pelvic pain focused anal sphincter relaxation [170]. is considered to be multifacto- erably due to different definitions of male sexual rial in that it can be a consequence of the cancer pain. treat- geographic region affecting rates [162–165]. neurolep- tics).g. One recent direction in research has been the study of anodyspareunia or the “recurrent or per. The history taking. tion including anal foreplay..g. prevalence rates vary consid- ing dyspareunia. a side effect of treatment. and vulvovaginal experienced persistent painful ejaculation [167]. cervical. Furthermore...F. Luzzi and Law [10] developed a definition ficulty in a large percentage of the men studied.g.g. or other life issues. 170]. and penile. calculi.. Relative contributions One common cause of sexual pain in men is of cancer compared to the treatment effects are ejaculatory pain due to CPPS. psychotro- pic medications (e. been noted in the literature including seminal and they make recommendations for pain reduc- vesicle disorders (e. and/or due to 3%. urethral stricture). genital. and pelvic majority of empirical studies examining cancer examination. medical conditions. and sexual functioning [168]. The prevalence often unclear [171].. and psychogenic factors. Lifetime prevalence rates range from 0. and lack of anal foreplay. degree of relaxation) tory of persistent or recurrent genital or pelvic [169. metastatic cancer). a commonly proposed four broad categories which can be reported hypothesized cause of the pain was diagnosed in men over the age of 18 with a his- psychological factors (e.174 C.1). Like the ISSVD classification system of Dyspareunia and the Cancer Patient vulvar pain. testicular. Pukall Sexual Pain Disorders in Men mirror female dyspareunia in a number of ways. have focused on sexual urine sampling. syndrome (CPPS). ment. role function and psychologi- Treatment-Related Side Effects cal factors. a . antidepressants. The authors propose that anodyspare- pain during sexual activity. They lubrication...

to maintain a certain degree of vaginal opening. . and perception of a shortened and/or inelastic vagina. reported symptom following risk-reducing especially if it is estrogen receptor positive [194. such as sexual pain in male cancer patients is that studies scarring. only more frequent in women who had received Currently. found that not recommended for women with hormone- compared to control women. anastrozole. however. penile cancer found that a small percentage matase inhibitors and is attributed to vaginal dry. tamoxifen. therefore nonhormonal lubricants should [184]. ectomy. Jenkins [182] also provided anecdotal reports of other conse.and silicone-based lubricants with respect to which treatment for cervical cancer are generally the first-line treatment for women results in more frequent dyspareunia. cancers [187–189]. One study with dyspareunia following cancer treatment. vaginal moisturizers such as vivors. and surgery for colorectal ing within the first few weeks following therapy. 193]. In the rare cases of vulvar cancer. scarring. start- transplantation [186]. vaginal swelling upon stimulation. trachelectomy. been documented in women following the use of One study investigating men after surgery for chemotherapy. In addition to carbophil moisturizers showed significant dyspareunia resulting from treatment of cancers reductions in dyspareunia following treatment affecting the sexual organs. and systemic effects. including respect to treatment strategies for dyspareunia extreme sensitivity to touch at the vaginal among female cancer survivors with the focus introitus and local burning with exposure to placed on topical therapies. effects of adjuvant treatment. apy for gynecological cancers are required to graft-versus-host disease after bone marrow perform graduated vaginal dilation [197]. adjuvant therapies for gynecological cancers can There have also been reports of pain with orgasm also lead to dyspareunia. comparing cervical cancer survivors to women however. ejaculation. Local estrogen cream semen. high rates of painful intercourse in women Women who have undergone radiation ther- following bone marrow transplantation [185]. there is no consensus on the safety of RT [183]. studies have found for breast cancer [196]. research has focused on following radiation therapy for prostate cancer the impact of local therapies including surgery [191]. dyspareunia was receptive-positive breast cancer [192. There has been a growing literature base with quences of RT for cervical cancer. be attempted first. such as painful ries. hormonal-based topical therapies are in the general population. than specific symptoms. experienced preoperative painful intercourse ness associated with reduced estrogen levels which resolved after treatment. or RT can result in decreased vaginal lubrication. or water. this line of treat- tomy can result in painful penetration due to ment has support from one study in which poly- scarring at the vaginal introitus. oophorectomy in women with ovarian cancer 195]. smaller percentage experienced newly acquired Although the use of chemotherapy and other painful intercourse following surgery [190]. Empirically. all of which can lead to Sexual Pain pain during intercourse [175–181]. and aro.12  Sexual Pain Disorders 175 number of studies have focused on the systemic As with the general literature on sexual pain. while an even following treatment [172–174]. there have been contradictory findings Replens®. vulvec. The sexual side explain the limited amounts of information about effects can be due to both local effects. One methodological concern that may and radiation therapy (RT). Dyspareunia has little empirical work has been done with men. In studies investigating only cancer sur. destruction of the vaginal epi- Treatment of Cancer-Related thelium. or pessaries. Dyspareunia is also a commonly hormone therapy for women with breast cancer. Treatment for cervical cancer with hyster. such as hormonal report on general ejaculatory problems rather changes following removal of the uterus or ova.

physicians may lack appropriate statistical manual of mental disorders. vivors may include discussing alternative sexual Fairley CK. Croft PR. individualized and multidisciplinary assessment Dilators can also be helpful in women following and treatment should be implemented. J Sex Educ Ther. Although there is evidence to indi. Hayes RD. PVD) or process and that follow-up related to sexual vaginismus. Pukall CF. New clinical and research perspectives on the sexual pain disorders. Binik YM. further research into these conditions vestibulitis syndrome as a pain disorder. The sexual pain disorders: a desexualized approach. The male sexual pain syn- and pathophysiology such that appropriate defi. Cohen DR. Dyspareunia is a common nology and classification of vulvodynia: a historical perspective. 200]. and furthermore. Khalife S. course (e. issues. although their likely that the causes of dyspareunia are multi- use can be replaced with regular sexual inter. Amsterdam and Krychman [199] recommend a multimodal approach to the treatment of sexual pain following cancer including pharmacother. Taffee JR. editors. Binik YM.F.g. In general. as sexual dysfunctions has been met with much 9. The classification of dyspareunia and vaginismus 2001. 1. 4. Meana M. therefore. Bennett CM. 3. Pukall The use of dilators is recommended over several on psychological and sexual functioning. J Reprod Med. 7. 1997.28:399–422. Law LA. 249–72. Pukall C. factorial and unique to each woman. condition among both pre. unia. feel uncomfortable or embarrassed in bringing Dyspareunia. 2006. Moyal-Barracco M. Washington.17:720–6. It is years in this population of women. 2004. Summer.5:777–87. DC: American Psychiatric training or experience in discussing sexual Association. dromes. sen. Binik YM. Text Revision. Dennerstein L. Obstet Gynecol. 4th ed. Fairley CK. Sexual counseling among cancer sur. Kao A. 11.2004.. Diagnostic and patients [200]. it is in reducing fear of pain during penetration and recommended that sexual side effects of treat- may help to prevent a cascade of events that can ment be discussed as part of the decision-making lead to long-term genital pain (e. Khalife S. Hayes RD. Systematic review of sexual problems: epidemiol- sual massage) in the context of a supportive ogy and methodology. editors. cate that these discussions are important to 5.90:497–505. Luzzi GA. . or building acceptance culties? Fertil Steril. is required to better understand their etiology 10. 2002. Khalife S. Summary 8.49:772–7. American Psychiatric Association. up these issues [201].2000. tions have an impact? J Sex Med. 2001. may also provide these benefits. J Sex Marital Ther. Kao A. 2.176 C. Jordan K. Fall M. sex therapy. patients themselves may 6.27:113–6.. Payne KA. Abbott FV. and that at fol. Bennett CM. and suggestions for specific problems. they are not asked about sexual concerns Biopsychosocial profile of women with dyspare- [185.25:36–44. Reissing ED. surgery for colorectal cancer or bone marrow Dyspareunia is also a common complaint among transplantation for hematological cancer [198]. NVA News. cancer survivors following both local and sys- The use of vaginal dilators may also be helpful temic treatments. course if a woman is partnered and interested. J Sex Marital Ther. can be made. 2003 ISSVD termi- ders. Pukall CF. cancer patients have reported that What is the “true” prevalence of female sexual dys- their physicians do not inform them of the sexual functions and does the way we assess these condi- side effects of cancer treatment. 2005. Segraves RT. mutual masturbation. possibly as pain disor. oral sex. low-up. Binik YM. Lynch PJ. Int J STD AIDS. Binik YM. 2008. intimate relationship. nitions and classification. Reissing ED.g. References apy. 2008. Lower urogenital tract pain and sexuality. of sexual activities other than penetrative inter. women and has significant and negative impacts In: Baranowski AP.90:583–9. Dennerstein L. In: Balon R. The regular use of Kegel exercises functioning be addressed. Abrams P. Glazer HI. Pukall CF. Assendelft WJJ.and postmenopausal 12. New York: Taylor & Francis. Khalife S. Goldfinger and C. In patients with cancer. Classifying vulvar criticism. Handbook of sexual dysfunction. Dunn KM. Are aspects of study design associated with the reported prevalence of female sexual diffi- positions to reduce pain. p.

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a ogy of ED. The launch on the market of oral phosphodi. the incidence of ED was 25% in 65-year- medical help. Italy incidence of 52% within a cohort of 1. Cancer and Sexual Health. except in some instances of traumatic or surgically induced ED. tile dysfunction (ED). in 1993. questioned [3]. In that of men reporting ED and eventually seeking report. Vita-Salute San Raffaele published in 1994. the minority of patients who report some form US National Institutes of Health panel on impo. which was then described Taking these aspects in mind.290 men J. which detailed an overall ED University. Saccà (*) Department of Urology. Kinsley et al. available on the epidemiology and pathophysiol- isfactory sexual intercourse [1]. These “historical” findings have been confirmed in a number of recent studies. Of major impor- tance in the field is the original report from the longitudinal Massachusetts Male Aging Study.1007/978-1-60761-916-1_13. However.). showing a decline in expectancy is progressively increasing.Chapter 13 Erectile Dysfunction: Prevalence and Pathophysiology Antonino Saccà and Francesco Montorsi Keywords  Erectile dysfunction • Prevalence • sufficient medical interest to lead to a search for Pathophysiology • NO • ET-1 • Testosterone an appropriate therapy only when it causes per- • Rho kinase sonal distress either to the patient himself or to the couple. Indeed. mainly addressing the important con- 3-month duration has been considered the mini. 20132 Milan. provided the first descrip- physician office visits for ED throughout the tion of the association between ageing as a bio- subsequent years [2]. even if it has Introduction been demonstrated that erectile function deterio- rates progressively with ageing. 183 DOI 10. ED becomes a matter of old men and 75% in men aged >80 year [4]. we overall sexual activity and erectile function qual- should expect a steady increase in the number ity coupled with the male ageing process. Epidemiology of Erectile esterase type 5 inhibitor (PDE5-I) therapy in Dysfunction 1998 was associated with a surge in resource use for ED. of ED will finally request treatment when tence developed the rigorous definition for erec. only a scarce It was roughly 20 years ago when. (eds. the aim of this as the persistent inability to attain and/or main. This definition is critical when evalu- ations of the prevalence of ED are considered. chapter is to briefly review the data currently tain a penile erection sufficient to complete a sat. Mulhall et al. mum length of time necessary for actual estab- lishment of the diagnosis. especially for ageing men.P. LLC 2011 . A. cept of the ageing man. © Springer Science+Business Media. as the mean life logic factor and ED [4]. as demonstrated by a 50% increase in In 1948. Current Clinical Urology. In this context. Likewise. Via Olgettina 60.

117   5.489   2. Similar results were reported by Grover et al. along with coronary artery several associated medical conditions.2 N/A not applicable .184 A.9% for men in 15%.5 11. 6.4 53.4 13. In addition. Similarly.779 10 – – – 78 Martin-Morales [14] 2001 Spain 2.9 – – 35. 6. diabetes. disease. increase in ED risk of all medical comorbidities age reached the status of an independent predic. In the National Health and lence and predictors of various types of sexual Nutrition Examination Survey database.1 33.1). hypertension. In 13 studies that within the same cohort of men. in a large population-based [21]. Saccà and F. all prevalence of ED was 51.7 – Koskimaki [12] 2000 Finland 2. Using the International Index of almost 1 out of 5 responders [7].240   8.9 37. ED complete ED tripled with ageing from 5. Saigal et  al. they demonstrated that car- addressing the presence of ED.7 23. with 10% of the study popula. ED remained constant at approximately 17%. the authors found diovascular disease.5% overall prevalence of ED of 49%. such as obesity. docu. however. increase to 67% impotent men when they were Diabetes mellitus resulted in the greatest aged 70 year.5 15. [5] 1998 USA 1. and the probability of minimal 40s. and a Table 13. Moreover. risk factors tor of ED even after adjusting for different clini.3 9. between 27 and 76% for men in their 60s.3% among people mented an incidence of ED of 18% in men 50–59 with diabetes [20]. the National Health smoking were also independently associated with and Social Life Survey. the over- dysfunction in both men and women. 77. who analysed a cross-sectional sample of study. strongest predictor of ED [8]. the probability of moderate ED doubled their 30s.7 4.7 – Rosen [15] 2004 Multinational 27. Interestingly.6 13. in multivariate analyses. study were impotent at age 40 year.476   1 1. included in the models. and cigarette cal variables [5].921 men aged 40–88 year referring to primary 20 year and older. defined as a of men aged 75 years or older reported some score lower than 26 at the IIEF erectile function form of ED [7].5 51. increasing age was the tion experiencing severe ED [5].4 Chew [9] 2000 Australia 1.178   – – 67 76 83 Glina [18] 2000 Brazil 825  2 9 16 27 49 Meuleman [10] 2000 Netherlands 1. between 16 and 67% for men in their 50s. between 9 and 39% for men in their from 17 to 34%. More recently. they recorded an dramatically increased in advanced age.839 11 15 22 30 37 De Boer [16] 2004 Netherlands 2. either undiagnosed hypergly- across all prevalence studies. adjusted for other factors.1  Prevalence of erectile dysfunction by decade of life [8] Decade of life 30–39 40–49 50–59 60–69 70–79 References Country n years (%) years (%) years (%) years (%) years (%) Feldman et al.7 – Mahmoud [11] 2000 Egypt 594 15.9 Ponholzer [17] 2005 Austria 2. Likewise.2 Kadiri [13] 2000 Morocco 646  5 – – 56.7 40 41.869   – 28. the probability of reported ED prevalence by decades of life. This prevalence Erectile Function (IIEF) [22]. self-reported ED affected care physicians. Montorsi aged 40–70 years. ED [5.5 69. after having been cemia or impaired fasting glucose levels.7 34.1 to was reported between 2 and 15. which assessed preva. with an 8–19] (Table 13.249   9 11 18 N/A – Braun [8] 2000 Germany 4.5 – 71. In their multivariable analyses domain.790   – 39 48 57 67 Laumann [4] 1999 USA 1. 8–19]. and An estimated 40% of the men included in the between 37 and 83% for men in their 70s [5. found that in men aged 3. years old [6].

vasoactive intestinal of the sex hormone milieu may significantly polypeptide. However. In addition. lead to relaxation of the smooth muscle cells within the walls of the penile arteries and sinusoids. In central erections. thus promoting the veno. damage to these structures has certainly been which become an isovolumetric reservoir. where synapses with parasympathetic fibres travelling back to the cor- pora cavernosa occur. to the lumbosacral cord. venogenic ED should be viewed as affecting the mitters involved in the erectile process [25]. problem both from the clinical and from the The same cascade of events is also seen with public health perspective. arteriogenic (failure to fill). reflexogenic. and hormones. and this is why in intracorporeal pressure and to penile rigidity. travelling finally along the initiate). occlusive mechanism. the dorsal nerve of the penis. sustaining penile rigidity until ejacu- lation or cessation of stimulation [26]. an the viability of cavernosal tissue [29. with the Ageing subsequent compression of the subalbugineal venular plexus against the inner surface of the The process of ageing may affect all the pillars of tunica albuginea. genating the corpora cavernosa and maintaining and nocturnal erections. abnormalities tors. in which the triggering ageing of the population [23]. occlusive mechanism of the corpora cavernosa. and a number of affect the quality of penile erections. When this mechanism is activated. However. arteries. Nitric oxide (NO). endothelial cells lining the walls sum. influenced by the availability of techniques for Further arterial inflow then leads to an increase identifying certain types of damage. anatomy and histology of the corpus caverno- In addition. nor. leading to alteration of the cavernous veno- of the cavernous sinusoids release active media. muscle contraction is stimulated with subsequent Currently. 28]. cavernous tissue. acetylcholine. The continuous stimula- tion of the penis occurring naturally during sexual Pathophysiology of Erectile intercourse contributes to maintain activation of Dysfunction the descending neural pathways to the corpora cavernosa. veins. including nerves. and this prostaglandins are considered the most impor. aspect has attracted much interest with regard to tant erectogenic neurotransmitters that ultimately its role in the ageing population [32]. Nocturnal Overview erections occur during rapid eye movement sleep from intrauterine life to late senescence and are Penile erection is a complex neurovascular phe. and veno- cavernous nerves. Based on the projected reflexogenic erections. They are believed nomenon under psychological control. male erectile system seem to play a leading role in epinephrine is released by neural adrenergic this regard. Relaxation of the intracavernosal sinusoids leads to blood filling the corpora cavernosa. terminal branches of genic (failure to store) [31]. Erections to represent a spontaneous mechanism for oxy- are usually classified as central. the term the cavernous nerves release several neurotrans. vascular and endocrine abnormalities affecting the When ejaculation and orgasm are achieved. 30]. Briefly. initial stimulus arising from supraspinal centres Abnormalities of erectile function have been travels through the spinal cord and reaches the traditionally classified as neurogenic (failure to corpora cavernosa. the erectile process.13  Erectile Dysfunction: Prevalence and Pathophysiology 185 formally diagnosed metabolic syndrome were fibres within the corpora cavernosa and smooth independently associated with ED. blood is evidence in the literature of ageing-induced actually entrapped within the corpora cavernosa. ED represents an important health penile detumescence. which sends signals portion of men in the twenty-first century [24]. The process of ageing is multifactorial . still poorly understood [27. it may be event is produced by mechanical stimulation of anticipated that it will affect an even larger pro.

Normal erectile function is a delicate who examined the role of the molecules involved balance between vasoconstrictor and vasorelax. [45]. inducing a substantial increase cGMP . Ageing also affects the genitourinary tract growth factor-beta1 (TGF-b1) [44]. which decrease the vasodilator penis of ageing male rats [41]..  13. However. fibres within the corpus cavernosum occur in the tion of fibrosis. Evidence suggests that unit of smooth muscle myosin phosphatase Fig. and cardiovascular [36] sys. of cavernosal smooth muscle relaxation. whereas ET-1. 21–24. duction of growth factors. in maintaining penile flaccidity. response. resulting The exact mechanism that links ageing to in inhibition of erection. another mech- smooth muscle dysfunction is not completely anism has been suggested by Chitaley et al. ED occurs [41–44]. including there are age-related alterations in the levels of but not limited to metabolic rate. being a potent G-protein that activates Rho-kinase. demonstrated Independent of the initiating factor. genetics.1  Nitric oxide (NO) pathway of erectile in intracellular cGMP. the latter modulators of erectile functioning when and environmental conditions [33]. Age-related smooth muscle dysfunction in 2002.186 A.1) and contraction mechanisms in the penis. Saccà and F. 40]. is believed to maintain Rho-kinase phosphorylates the regulatory sub- penile flaccidity [39. Montorsi in nature and depends on several factors. a small monomeric relaxation. NO derived from the endothelium or ation via sequestration of intracellular calcium (Ca2+) cavernosal nerves signals guanylate cyclase. Rajasekaran et al. 26. recorded age-related impairments in the has long been recognised in the respiratory [34]. Garban et  al. causing smooth muscle relax- function [112]. Endothelium-derived NO (Fig. the ultimate that decreased nitric oxide synthase (NOS) activ- common pathologic process is damage to smooth ity and a reduction in NOS-containing nerve muscle cells and an increase in the accumula. understood. Activated vasoconstrictor agent. This key regulator of cavernosal smooth muscle pathway involves RhoA. 46]. ant mediators on corporal smooth muscle tone Besides the well-established noradrenergic [38]. an addi- endothelin-1 (ET-1) have been individuated as tional mechanism involving increased sensitivity modulators of erectile function. Phosphodiesterase type 5 breaks down monophosphate (cGMP).  13. NO is a to ionic calcium has been proposed [45. lifestyle. expression of NO and ET-1 as well as in the pro- gastrointestinal [35]. Defects in and is associated with lower urinary tract symptoms the production or release of neurotransmitters or [37] and sexual dysfunction [4–7. which in the endoplasmic reticulum and inhibition of Ca2+ then converts guanosine triphosphate to cyclic guanosine ion channels. such as transforming tems. 29] the presence of antagonists could cause inhibition in both men and women.

oxygen species (ROS) plays a fundamental role trict begins earlier because of the small size of in the natural ageing process [65–67]. The inter- the penile vessels and can anticipate severe action between ROS and NO has been indicated vascular and coronary symptoms: ED can be as crucial to the development of ED [68]. expandability. is associated with elevated advanced stages. in more factor for ED [49. which may be responsible for the impaired observed in the ageing male [63]. Moreover. as a conse- been recognised as a well-known vascular risk quence. the erectile tissue loses its penile RhoA levels [51]. which is associ- mary. because of the beneficial in attenuating the decline in erectile down-regulation of the expression of the consti- function in hypertensive rats [52]. ments to Ca2+ [47]. This phenomenon is mostly would be an increased penile smooth muscle responsible for the veno-occlusive dysfunction tone. which has been reported to and hypercholesterolemia. smooth muscle atrophy. glycans. An age-related increase in fibrosis. NO interacts with superoxide to In animal models mimicking pelvic ischemia form peroxynitrite. real fibrosis. 60]. smooth muscle and in the development of corpo- associated vascular disorders [48]. are early and severely involved by ath. branches. and this over-expression has also involved in the deterioration of cavernosal been suggested as being responsible for age. In addition. nism recently suggested as a potential factor in erosclerotic lesions [56].13  Erectile Dysfunction: Prevalence and Pathophysiology 187 (SMPP-IM). which has flow to the corpora cavernosal and. inhibitor in rats has been shown to induce penile this process results in decreased arterial blood erection [45]. [58] demonstrated remains the leading cause of death in the adult that – at least in the rabbit – the level of TGF-b1 population [54. In the . pelvic atherosclerosis may able to relax vascular and non-vascular smooth damage the pudendal-cavernous-helicine arterial muscle. According to the artery the pathogenesis of ED in the elderly. Azadzoi et al. and noncompli- RhoA expression has been documented in rat ance of the bladder [58]. Chronic ischemia is also responsible of the over-expression of TGF-b1. In the early stages of atherosclerosis. and Rho-kinase. This protein is a pleotropic cytokine demonstrated to be an essen- tial mediator of tissue fibrosis [49]. hypertension. In sum. Moreover. leads to ED [60]. ET-1. play a central role in atherogenesis [69]. However. inhibition of capability to produce the quantity of NO needed Rho-kinase activity has been demonstrated to be for smooth muscle relaxation. such as NO. In turn. 55]. damage to the vasculature caused by reactive the atherosclerosis involvement of the penile dis. chronic ischemia resulted in muscle contraction. Inhibitory phosphorylation of strated an evident similarity in the smooth muscle SMPP-IM leads to the sensitisation of myofila. the net result of the impairment of erection ated with an impairment of the corpora regulators. and intracavernosal injection of this tree [61]. Vascular Disease Overproduction of TGF-b1 decreases the smooth muscle-connective tissue ratio by inducing the A further significant mechanism suggested as a expression of collagen. while inhibiting the growth of smooth Atherosclerosis-induced arterial insufficiency is muscle cells and the activity of collagenase [64]. tutive NOS [62]. which in turn may lead to ED [30. and proteo- potential cause of ED is pelvic atherosclerosis. fibronectin. a common clinical problem in the elderly and In this context. especially the bifurcation of the iliac Oxidative stress is another important mecha- arteries. which translates into smooth In their report. alterations of the detrusor and of the corpora. Chronic ischemia is vascular tissues. considered the “tip of the iceberg” [57]. 50]. Chitaley et al. The abdominal aorta and its correlates with the severity of the fibrosis. showed that a specific inhibitor of Rho-kinase is 59. erectile response seen in the ageing rats. demon. Oxidative size theory proposed in 2003 by Montorsi et al. tent in the corpus cavernosum.. In addition. Azadzoi et al. Specifically. elderly men are Rho-kinase appears to be effective in reversing subjected to a decrease in smooth muscle con- ED in castrated hypogonadic rats [53].

other hormones are involved in LH suppression. In healthy gametogenesis [77]. and 156  ng/dL for men in their decreased libido and erectile quality. 196. 81. when clearly symptomatic. leading to bioavailable testosterone owing to a decrease in a further decrease in available NO. it is still questionable and Several hormones are affected by constant unclear whether the reference range of serum decrease throughout the ageing process. decreased lean body mass. and impaired cognitive which in turn results in a further increase of function). Mohr thyroxine. fatigue. extensively described. healthy males. such as estrogens and DHT. the role of oxidative patients aged 70–79 years [78. 215. . decreased 40s. and growth hormone [81].188 A. Finally. androgens derived from younger men is also ing testosterone. Several other fraction is transported by albumin and authors showed that a proper endocrine milieu is other plasma proteins [87]. et  al. melatonin. Testosterone dysfunction? represents the major secretory product of the testis and is the primary inhibitor of LH secretion in men [86]. consequently of 1. in turn. the levels of such a deficiency has recently been renamed total and free testosterone decrease with age symptomatic late-onset hypogonadism [78–80]. respectively. Bioavailable testos- necessary for penile function: An alteration of one terone. acterised by a gradual decline in serum total and dence of apoptosis in the endothelium. Briefly. 2% of testosterone is free in the blood. which react with a vasoconstriction stimulus [81–83]. In ageing men. 85]. and 70s. 84. dehydroepiandrosterone (DHT). stress in the corpora cavernosa is a critical deter. Saccà and F. However. as previously mentioned. and increased insomnia. depressed memory. the normal testosterone range is 300– of the androgen production – and. Endothelial closed loop of feedback control mechanism mod- dysfunction represents the first step in the ulating and maintaining reproductive function. 30% is bound to the sex- The endocrine status plays a significant role in the hormone-binding globulin (SHBG). an alteration subjects. and the regulation of erectile function/dysfunction. [89] have thus suggested age-specific Symptomatic hypogonadism is associated with thresholds for defining hypotestosteronemia: numerous symptoms and signs. the testicular Leydig cell number and in their releas- reduction in NO concentration increases the adhe. decreased body hair and concentration of the available NO [70]. [89]. corresponding to 10. the enzyme responsi. ble for inactivating superoxide is inhibited. which is the fraction of testosterone not or more hormones can be the cause of ED [74–76]. it is char- peroxynitrite and superoxide increase the inci.4–34. decreased peroxynitrite and may drive a reduction in the mineral bone density. bound to the above reported proteins. Moreover. 60s.7 nmol/L the circulating levels of sex steroids – has been in most assays of serum total testosterone [88]. Endocrine Factors In normal. Moreover. Therefore. The prevalence of hypogonadism has mediated by thromboxane A2 and leukotrienes been addressed in several longitudinal studies and [71]. represents Hypogonadism has been defined as a state of the cornerstone of androgen function. the hypothalamic-pituitary-gonadal system is a minant in the pathophysiology of ED. in pathophysiology of ED and can anticipate a major this context. includ. deficiency in gonadal function made manifest by changes in SHBG concentration are responsible deficient secretion of gonadal hormones and/or for androgen function regulation. Because the reduced availability of NO and has been recorded in 2% of men younger than 50 long-term endothelial damage are the two most years of age. However. skin. Montorsi presence of peroxynitrite. effects on the secretion of luteinising hormone (LH) FM/AS: a paragraph or two on endothelial and follicle-stimulating hormone. among them are 251. appropriate for the elderly population. the gonadal hormones have inhibitory peripheral vascular problem [72.000 ng/dL. intellectual capacity (along with depression. 73]. while it ranges from 34 to 70% in important causes of ED. 50s. ing capacity as well as an age-related decrease in sion of platelets and leukocytes to the endothelial episodic and stimulated gonadotropin secretion cells.

were probably the first ing appears to be a slowly progressive disorder. is part of the and. In castrated rats. Prostate Suppl. Furthermore. In con- Chamness et al. 1. 1948. [90] demonstrated that the activity trast. 2. recent studies highlighted the interaction testosterone – most probably play a significant between testosterone and PDE5-Is [102–106]. Disease in the United Neurological Factors States. libido. and male sexual function. Sexual behaviour in the human male. animal studies demonstrate that Conclusions testosterone may facilitate erection in the dop- aminergic mesolimbic cortex. replacement can recover its production. responsible for It seems reasonable to hypothesise that the age sexual arousal [96]. both the result of atherosclerosis-induced cavernosal libido and the frequency of spontaneous erections ischemia. outlet. rapid increase in sexual activities [110]. the use of dopaminergic agonists nism of NO-mediated vasodilatation in the penis in the treatment of hyperprolactinemia showed a and in other organs [90–93].270:83–90. 1993. alone. sexual activity. Kinsey AC. ejaculation. NIH.10:9–13. in turn. Indeed. standpoint is the role of the dopaminergic sys. and this can anticipate improve- and spontaneous erections. Again. dopamine-blocking agents often reduce of NOS is reduced by 45% and that testosterone sexual response. In: Kinsey AC. ual function and positively correlated to that editors. [109]. Slob AK. US Renal Data System. short-term testosterone administration was able to increase serum levels of both T and free T. Age. National Institute of Diabetes and Digestive and Kidney Diseases. 2006. 2000. In human subjects with phar- link in ED may be mostly considered as the macologically induced hypogonadism. Martin CE. [108]. for instance. References fil. Prolactin is another neurotransmitter that testosterone is implicated in the modulation of plays a key role in the CNS regulation of the alpha-adrenergic vasoconstrictor activity [94. indeed. USRDS. Prolactin. Pomeroy WB. Bethesda: National Institutes of Health. Also of importance from the pathophysiology 3. 4. which ultimately leads to both severe decreased. JAMA. likely by increasing arterial inflow to the penis during sexual stimulation [107]. Age and sexual tem. Pomeroy PW. defined as non-responders to sildenafil the development of veno-occlusive dysfunction. In this con- of hormones controlling sexual organs – mainly text. to clearly show that in a small group of patients it seems wise for the patient to seek medical with arteriogenic ED and low to normal androgen intervention earlier rather than later to minimise levels. Moreover. Consensus development panel on impotence. These alterations have been demon- cavernosal fibrosis and eventual veno-occlusive strated to be reversible after restoration of normal dysfunction. Abnormalities in circulating levels blood levels of testosterone [97–101]. Animal data suggest ments in neurologic activities and symptoms that testosterone may play a role in the mecha.13  Erectile Dysfunction: Prevalence and Pathophysiology 189 Testosterone is therefore a key factor in sexual Parkinson’s disease demonstrate an increase in function and is necessary for libido. Patients suffering from hyperprolactine- venous occlusion mechanism responsible for the mia may primarily complain of ED [111]. . Martin CE. As the ED of age- Aversa et al. 2006 annual data report: atlas of end-stage renal. which seems to be closely involved in sex.. Patients treated with l-DOPA for Philadelphia: WB Saunders. testosterone is involved in cen- tral nervous system (CNS) control of the erectile pathway. these results being coupled with a significant improvement in the erectile response to sildena. role at least in some patients. 95] erectile pathway. maintenance of erection [96]. can enhance erections by attenuation hypothalamic-testicular-pituitary axis implicated of vasoconstriction and by contributing to the in ED.

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