Roy J Levin
While males have little or no difficulty in having and identifying their orgasms, this cannot be said for a significant proportion of women. Two topics of female sexuality and its dysfunctions, the difficulty in inducing orgasm, especially through coitus, and recognizing that an orgasm has occurred, have been discussed at length.
It is often stated that for men orgasm is the hoped-for goal whenever they initiate a sexual scenario, but that this is not the case with women. Women, it is claimed, value the “afterglow” of the sexual arousal and the physical intimacy of being cuddled as much as the orgasm.1,2 In one survey, admittedly questioning self-selected women subjects, affection, love, and intimacy were given as the major reasons for liking coitus, with the act of penetration rather than orgasm per se as their favorite sexual experience.3 These American studies were undertaken some 30 years ago, and, as the sexual perceptions and attitudes of individuals and societies change, their conclusions may not now be valid. In fact, orgasm and its difficulties have been claimed as the second most reported sexual problem for women.4 A study conducted in 1992 looked at the relationship between sexual enjoyment and orgasm in couples attending university.5 It was reported that “nothing in the data supports the cultural stereotype that orgasms are more important to men than to women.” When asked whether “sex without orgasm cannot really be satisfying” in a recent, statistically valid, national survey of British sexual behavior, approximately half of the men (48.7%) agreed that orgasm was necessary to male sexual satisfaction, and when women were asked, some 43% also agreed that this was so for men.6 When the question was asked in relation to women, 37% of men agreed, while 29% of women also agreed with the statement. Thus, nearly a third of women, a highly significant percentage, do think orgasm is important. Apart from the obvious reward of its ecstatic pleasure, the physiology of female sexual arousal may be the reason for women desiring orgasm. Sexual arousal creates hyperemia and vasocongestion in a wide number of female pelvic structures (uterus, vagina, clitoris, urethra, labia, pelvic ligaments, and even possibly the fallopian tubes and ovaries), giving rise to an uncomfortable feeling of “pelvic fullness” (see Chapters 5.1- 5.6, 6.1, and 6.2). Its dissipation is very slow, even with orgasm, which facilitates the action, although a single orgasm does not usually cause complete dissipation.7 Orgasms, however, are the natural and pleasant means to ameliorate the pelvic discomfort.
Objective specific indices of the female orgasm
“How does an orgasmic-naive woman know that an orgasm has occurred?” Levin8 discussed the problem by asking, “Who defines what an orgasm is?” The subjective experience of orgasm (ecstasy, euphoria, and extreme pleasure) is normally accompanied by physiologic body changes, a number of which have been used to indicate that an orgasm is impending, is occurring, or has occurred. The descriptions of many of these changes come from the classic observations of Masters and Johnson7 nearly 40 years ago, but a few newer ones have been added since. These specific objective indicators which occur either just before, during, or after the female orgasm are listed in Table 6.4.1. They have been discussed critically and fully in a recent review on the female orgasm.9 The most quoted physical indicator for the occurrence of an orgasm is that of contractions of the vaginal/pelvic striated muscles (see Chapter 4.4 in this volume), but some women say they have orgasms without experiencing such contractions, although they may be weak and thus women are unaware of them.9,10
Table 6.4.1. Specific objective indicators of the female orgasm
Typologies of female orgasm
Early psychoanalytic opinion about the female orgasm (see Chapters 1.1, 3.1, and 11.1) proposed a dual typology; because they were easier to obtain, those obtained by stimulation of the clitoris were regarded as “less mature”, the only authentic orgasms being those obtained through vaginal coitus.11 This duality developed into the concept that female orgasms were obtained from either clitoral or vaginal stimulation. The literature abounds with descriptions and discussion of vaginal as opposed to clitoral orgasms.7 Anecdotal reports from women revealed that those obtained from the clitoris used descriptions employing the words “warm”, “ticklish”, “electrical”, and “sharp” whereas those from vaginal stimulation were more often referred to as “throbbing”, “deep”, “soothing”, and “comfort- able”.12 Kinsey et al.13 and Masters and Johnson7 reported that the vagina had few sensory receptors and that some clitoral stimulation would occur from penile thrusting during coitus. Moreover, according to Ingelman-Sundberg,14 the vagina acts like a hummock around the urethra, so that during vaginal coitus, the penis stretches two of the ligaments inserted around the base of the clitoris (see Chapters 4.1-4.4). Thus, coitus should always create a mixture of vaginal and clitoral stimulations. If this is true, the anatomic basis of the different feelings is puzzling unless we accept that, mentally and emotionally, coitus (where the vagina is distended) and stimulation of the clitoris per se are likely to be appreciated differently.10,15 Masters and Johnson7 posed the question: are clitoral and vaginal orgasms truly separate anatomic entities? Their answer was an unequivocal “no”. They stated “from an anatomic point of view there is absolutely no difference in the responses of the pelvic viscera to effective sexual stimulation regardless of whether the stimulation occurs as a result of the clitoral-body or mons area manipulation, natural or artificial coition, or, for that matter, specific stimulation of any other erogenous area of the female body”. Most of their changes that supported this statement came from direct observations with few physiologic measurements. More recent physiologic recordings of uterine smooth muscle and pelvic striated muscle contractions during orgasms induced by stimulating either the anterior vaginal wall (G spot) or the clitoris have revealed different patterns of contractions of these muscles, suggesting that there may well be objective evidence of at least two types of orgasmic response created by the stimulation of different genital sites. A set of these myographic recordings by John Perry is shown by Levin.16
A frequently quoted typology is that of Singer,17 a philosopher without any experience in laboratory studies, who proposed three types of orgasm from published descriptions: (1) “vulval”, showing rhythmic contractions of the vagina activated by clitoral or coital stimulation; (2) “uterine” , without vaginal contractions but accompanied by apnea and gasping activated during coitus and largely due to penis-cervix contact; and (3) “blended”, containing elements of both vulval and uterine orgasms activated by coitus and accompanied by apnea.
Singer’s evidence for this typology relied on remarkably limited scientific observations obtained from a very few subjects, and he used a novelist’s description (see Levin16 for extended critical discussion). The importance of cervical stimulation by the thrusting penis in this typology was not about stimulating the organ per se, but of its displacement, causing it to rub against the peritoneal membrane claimed to be “a highly sensitive structure”.18 However, a recent review of the cervix in sexual arousal concluded that the evidence for or against its involvement in orgasm was weak and that observational studies could not answer the question.19
John Perry and Beverly Whipple, in The G-Spot and Other Recent Discoveries About Human Sexuality, proposed an interesting “continuum schema or typology” for the female orgasm that incorporated Singer’s categories but added those originating from the G-spot (anterior vaginal wall) stimulation.20 At one end were orgasms produced by clitoral stimulation that created rhythmic contractions of the pelvic muscles (mainly mediated through the pudendal nerve), while at the other end were those produced from stimulation of the G-spot (mainly mediated through the pelvic and hypogastric nerves), which expressed uterine contractions (see previous description above of Perry’s myographic data). In the middle were the two types of orgasm that probably occur most often. This “continuum” typology, however, did not catch on.
The most recent typology for female orgasms was developed by Bohlen et al.21, using the different types of vaginal contractions recorded during laboratory studies of orgasm. They divided orgasms into those that had regular rhythmic contractions (mean duration of orgasms about 13 s), those that had regular contractions with later irregular ones (mean duration 51 s), and those that had no regular rhythmic contractions during their orgasms (mean duration of orgasm 24 s). The differences in the duration of these orgasms are remarkably large: Levin and Wagner, who timed the orgasms of their 26 laboratory subjects, recorded a mean (±sd) duration of 19.9 ± 12 s.22 Unfortunately, only 11 nulli- parous subjects were studied by Bohlen et al.21, and no other confirmatory studies have been published. A general classification of female orgasm built on such a limited number of subjects must remain sub judice. Mah and Binik23 have discussed the variability of human orgasmic expression in terms of typologies.
Functional imaging of the brain at orgasm
One of the more recent and exciting technological advances in sexual arousal studies has been the use of functional brain imaging to identify which areas are activated or inhibited by sexual behaviors. A number of studies on sexual arousal and orgasm (ejaculation) have been carried out in men, but few so far in women. Holstege et al.24 used blood oxygenation level-dependent positron emission tomography to record the various parts of the brain involved in ejaculation (and thus orgasm) in men during an observational window of some 60 s (see Chapter 10.2). A large number of sites were found to be highly active - the mesodien- cephalic transition zone, including the ventral tegmental area, midbrain lateral and central field, zona incerta, subparafaccicu- lar nucleus, thalamic nuclei (ventral, posterior midline, and intralaminar), cerebellum, lateral putamen, and claustrum - while there was neocortical activity in Brodman’s areas 7/40, 18, 21, 23, and 47. Two sites were deactivated, the amygdala and the entorhinal cortex, while the hypothalamus showed (during the short period of observation) no activity (see Chapters 5.2 and 5.3). The reason for detailing these sites in men is that Holstege,25 at a recent conference, reported that the pattern of activation of these sites was similar during orgasm in women except for two outstanding differences: first, the amygdala was active in women and not deactivated; second, the periaqueductal gray area was activated, but this was not seen in men.
One of the difficulties in interpreting these data is that many of the brain areas apparently involved in arousal/orgasm are also known to be involved in other body functions. The amygdala, for example, is involved among other things in anxiety, fear, and anger, while the periaqueductal gray area receives input from the amygdala, lateral stria terminalis, hypothalamus (medial and lateral), preoptic region, and parts of the prefrontal cortex. It sends its outputs to the spinal cord directly and indirectly, and these are involved in nociception control, micturition, vocalization, and pupil dilation. The most interesting of these, perhaps, is the nociception control, with the stimulation of periaqueductal gray area creating an analgesic effect. Vaginal self-stimulation has been claimed to raise the pain threshold in women, while the induction of orgasm further raised it, both without changing tactile sensitivity.26 Thus, activation of the periaqueductal gray area during female orgasm may well be through this mechanism.
Development of pleasure from orgasms
Two opposing views of obtaining orgasmic release are that it is simply a reflex involving a stimulus-response reaction,27 or that the sensations of orgasm have no immanent meaning attached to them and that they are identified by women as “orgasm” because of the situation in which they occur rather than due to specific connection between sensory inputs and the brain. It is thus a “learned” activity.28 Mead observed, “the human female’s capacity for orgasm is to be viewed more as a potentiality that may or may not be developed by a given culture” and “the capacity to learn a total orgasmic response is present differentially in all women.”29 Certainly, the pleasure associated with coitus and its orgasms appears to be a learned activity.10
Why do women, but not men, have multiple serial orgasms?
One obvious difference between orgasms in men and women is that women can have multiple serial orgasms,10 with the latter ones being as good as or even better than the first. Most males have a post-ejaculatory refractory time. It has been proposed that the release of prolactin at the time of orgasm causes the post-ejaculatory refractory time in men, but women do not experience this. Presumably, prolactin released at orgasm acts differently in women.30
The arousal sites to trigger orgasm
The induction of female orgasm can occur from a variety of anatomic sites. These include the major ones of the clitoris (especially the glans) and the vagina (especially the anterior wall that includes Halban’s fascia, the urethra, and the G-spot), but orgasm can be obtained by stimulation of the periurethral glans area (the area surrounding the urethral meatus), mons, or breasts/nipples by mental imagery or fantasy, or even by hypnotic suggestion. Kinsey et al.13 reported that orgasm could occur even from bizarre stimulations such as that of the teeth or blowing on the hair of subjects. Consciousness is not a requirement, as orgasm is known to occur during sleep.
Putative roles of orgasm in reproduction
In no other area of the female orgasm has so much been attributed with so little scientific evidence. Time and again authors repeat the mantra that the contractions of the uterus induced at orgasm will facilitate sperm transport by increasing the rate at which they will be moved along the female genital tract. This faster transport, it is then said, will aid fertility. The reality, however, is that the fastest sperm transport in the female genital tract is observed in the nonaroused female! This has been shown experimentally.31 Rapid sperm transport during coitus has been inferred from the results of Settlage et al., who actually studied their transport in anesthetized women during surgery.32 While their findings have been equated to what occurs during coitus in the sexually aroused women, the two conditions are entirely different and cannot be compared. Levin has described the differences and why the conclusions from the experiments are physiologically invalid.33 In fact, as the women in the Settlage et al.32 experiments were anesthetized and thus could not be sexually excited, they would indeed have shown the rapid transport of sperm as expected. The scenario during coitus is quite different. Sexual arousal causes vaginal tenting to occur, elevating the cervix well away from the vaginal posterior wall and the ejaculate. Under these conditions, uterine contractions would have no effect on sperm transport because the cervix is not in contact with the semen. Only when resolution of the sexual arousal occurs does the cervix get immersed into the now liquefied seminal pool. Levin has described this scenario in detail and the importance to reproduction that delaying the sperm transport creates.34 Orgasm, by hastening the descent of the cervix into the seminal pool, may not be the most facilitatory factor in fertilization. There is, however, some evidence that after arousal/orgasm the female genital tract has an inhibited motility.34
Baker and Bellis35 made a number of provocative suggestions, based on their studies of the amount of leakage of semen from the vagina (termed “flowback”), about how the occurrence and timing of female orgasm in relation to copulation and male ejaculation influenced the number of sperm retained at both the current and next copulation.
Orgasms were claimed to generate a “blow-suck” mechanism that could take sperm or acid vaginal contents into the cervical fluid, thus affecting sperm viability. A chosen orgasm strategy could be used to facilitate pregnancy from a particular desired partner, not necessarily the husband. These suggestions and conclusions are controversial and have yet to be accepted or confirmed by others.34
Why do women have contractions of their pelvic muscles at orgasm?
Males need striated muscle contractions to forcefully eject their semen.36 Many women, although not all, experience striated pelvic muscle contractions at orgasm, but their function is unknown. The contractions may cause the pleasure experienced at orgasm, but simply contracting muscles voluntarily does not yield ecstasy. The contractions may dissipate the pelvic vasocongestion induced by arousal, but multiple orgasms would be needed to evacuate the blood congestion. The contractions may be for expressing the female urethral expulsions. Not all females have urethral expulsions (from the periurethral glands), and in those that do, the volume expelled is normally around 0.5 ml. Powerful striated contractions are hardly necessary for such a volume. However, it is possible that the contractions serve a “housekeeping” function, “sweeping” out any residual or buildup of secretions in the urethra, although subsequent urination would suffice. It is possible the contractions serve to excite the male to ejaculate during coitus, thus capturing his sperm. This would be a reproductive function, but most males have ejaculated before females have their coital orgasm. Finally, the contractions could simply be an example of a “biological spandrel”37 - a mechanism, function, or structure that has no apparent function in one sex but is present because it is essential in the other. The striated musculature of the pelvis stems from a common fetal prototype. While its contractions at orgasm may have no function in the female, they do no harm.
Vocalizations at coitus and orgasm
Both males and females make involuntary sounds during high levels of sexual arousal and at orgasm, conveying the acceptance, the effectiveness of the sexual arousal, the pleasure induced, and the approach and arrival of orgasm.38 These erotic sounds made by the female are highly exciting to males and enhance their arousal, thus facilitating ejaculation and the capture of the semen. Apart from this, Passie et al.39 have suggested that the groaning and hyperventilation can create hypocapnia (lowered plasma partial pressure of carbon dioxide) that reduces cerebral blood flow mainly in the neocortex gray matter rather than in the limbic structures. The imbalance may intensify the emotional states of the sexual experience.
Arousal and orgasm in nonconsenting subjects
When both parties are willing to partake in sexual stimulation, the outcome of sexual arousal and orgasm is usually welcome. Thus, the mental state of the parties is one of happy acceptance of the arousal and the orgasm(s) to come. Without this state, it is often thought that arousal and orgasm would be difficult to achieve. What happens, then, in the case of nonconsenting women subjected to sexual stimulation through force, fear, or an impaired state of consciousness (sleep, drug, alcohol, or hypnotically induced)? Levin and van Berlo40 posed the question of whether or not the female can experience sexual arousal and orgasm involuntarily or even against her will. Upon review of the topic and its limited literature, Levin and van Berlo40 concluded that such stimulation can and does lead to unwanted arousal and even orgasm, but that such outcomes cannot be used as a sexual assault defense to imply that the subject consented to the stimulation.
The pathophysiology of female orgasm
Nosology and terminology
The nosology of women’s sexual disorders is formalized in the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders (DSM), fourth edition (DSM-IV- TR),41 and in the International Statistical Classification of Diseases and Related Health Problems (ICD-10).42 The diagnostic criteria in relation to orgasmic dysfunction are shown in Table 6.4.2 from the DSM, and from the ICD-10 classification of mental and behavioral disorders diagnostic for research by the World Health Organization. Both rely on the sexual response cycle as described by Masters and Johnson7,43 and modified by Kaplan.27
There has been increasing criticism of this nosology and even a recent attempt to modify the definitions of female sexual dysfunction by a 17-member international consensus committee,44 who stated: “Orgasmic disorder is the persistent or recurrent difficulty, delay in, or absence of attaining orgasm following sufficient sexual stimulation and arousal which causes personal distress.” Even the deliberations of this group failed to satisfy the critics.45 More recently, a second, self-selected group, comprising seven of the previous one with six new participants, have made further suggestions to revise the previous revision in the light of a burgeoning evidence-based movement. However, as they state, many of the suggested revisions and expansions will need to be tested for validity and usefulness in the clinical setting. The methodological difficulties of characterizing female sexual dysfunction in relation to definitions (see previous comment), assessment (use of self-reported data), and type of population (selection bias, prevalence, and incidence estimates) have been discussed at length in another committee report published in 2000,46 and they will not be repeated here. One difficulty with the diagnostic criteria of DSM-IV is that if a woman is diagnosed as having an orgasmic disorder, it precludes her from having a sexual arousal disorder, but, in reality, many women with orgasmic disorders also have arousal disorders.47 Indeed, comorbidity seems to be the usual condition of female sexual dysfunction(s) rather than its being isolated into the specific diagnostic categories.48 Other complications involve terms such as “lifelong versus acquired” and “generalized versus situational circumstances”. It is not always clear whether a secondary disorder is acquired under any circumstances. There are serious problems with the whole concept of female sexual dysfunctions, even to the extent that some authors claim that they are influenced too much by the needs of the pharmaceutic industry.49,50
The assessment and subsequent treatment of orgasmic dysfunction by Masters and Johnson43 was a milestone. They diagnosed a woman as having “primary orgasmic dysfunction” if she reported lack of orgasm during her entire life span, whatever the method used to try to induce an orgasm. If a woman had experienced at least one instance of orgasm, regardless of the method of stimulation used, she was classified as having “situational orgasmic dysfunction”. Three arbitrary categories of this dysfunction were defined further: masturbatory orgasmic inadequacy, where the woman is unable to achieve orgasm by masturbation even though it has occurred during coital activity; coital orgasmic inadequacy, where the woman is unable to achieve orgasm through coitus, although she is orgasmic through masturbation by herself or her partner; and random orgasmic inadequacy, where the woman has had coital and/or masturbatory orgasms, but they are rare and usually unexpected.
While the term “primary orgasmic dysfunction” has remained in the clinical literature, the situational dysfunction has been renamed “secondary orgasmic dysfunction”. The term “frigidity” has disappeared from the literature,51 but the term “anorgasmia” is used for persistent and recurring difficulty in achieving orgasm.
Prevalence of impaired orgasm
The prevalence of orgasmic dysfunction in a statistically valid sample of the general female population has been difficult to ascertain. Recently, Bancroft et al. undertook a national telephone survey of female distress about sex in their heterosexual relationships over an age range of 20-65 years.52 They reported that 9.3% of their sample had “impaired orgasm” (not specifically defined), and they compared this with four other surveys undertaken in 1988-99, which quoted a prevalence of “impaired orgasms” of 16-27%. Thus, orgasm difficulties, as reported by the women’s own assessments, are probably around 9-27%.
Table 6.4.2. Diagnostic criteria for orgasmic dysfunction from DSM-IV and ICD-10 DSM-IV: Female orgasmic dysfunction (302.73)
1. Persistent or recurrent delay in, or absence of, orgasm following a normal sexual excitement phase, Women exhibit wide variability in the type of intensity of stimulation that triggers orgasm the diagnosis of female orgasmic disorder should be based on the clinician's judgment that the woman's orgasmic capacity is less than would be reasonable for her age, sexual experience, and the adequacy of sexual stimulation that she receives.
2. The disturbance causes a marked distress or interpersonal difficulty.
3. The orgasmic dysfunction is not better accounted for by another Axis 1 disorder (other than a sexual dysfunction) and is not due exclusively to the direct physiological effects of a substance (e.g., a drug of abuse, a medication) or a general medical condition.
CD-10: Orgasmic dysfunction (F32.3)
1. The general criteria for sexual dysfunction (F52) must be met.
2. There is orgasmic dysfunction (either absence or marked delay of orgasm) which takes one of the following forms:
(i) orgasm has never been experienced in any situation
(ii) orgasmic dysfunction has developed after a period of relatively normal response
(a) general orgasmic dysfunction occurs in all situations and with any partner;
(b) situational for women, orgasm does occur in certain situations (e.g., when masturbating or with certain partners).
Causes of orgasmic dysfunction
It is said that 90% of female orgasmic difficulties arise from psychologic/sociologic causes: poor sexual communication and knowledge, inadequate or unsuitable stimulation, poor relationships, traumatic early sexual experiences, and mental conditions (mood disorders or mental illness). Some of other possible causes of orgasmic dysfunction are listed in Table 6.4.3 (see Chapter 9.4).
Although disorders of orgasm have been treated by a variety of methods,53 extensive empirical outcome research for controlled and uncontrolled studies is available mainly for cognitive behavioral approaches and less so for pharmacologic approaches (see Chapter 11.4).54 These will be described briefly. In general, the hierarchy of successful treatment is that it is greatest with self-induced orgasm, less with partner-induced orgasm by manual or oral stimulation, and least with coitus without any other stimulation. Outcome is also better for women who have never had an orgasm than for those with a desire to increase orgasms with partner sex.
For a review of the field of sex therapy, the analysis of Schover and Leiblum is very critical as it claimed that the field was in the doldrums.55 In the case of the treatment for female orgasmic disorder, they argued that all the major components were present in the 1970s and few new treatments had been added. Furthermore, outcome research, especially long term, was conspicuously absent.
Table 6.4.3. Some nonpsychologic causes of female orgasmic dysfunction
1. Neurological disorders
Damage to sacral/pelvic nerves, multiple sclerosis, Parkinson's disease, narcolepsy, epilepsy, spina bifida, amytrophic lateral sclerosis
2. Surgical conditions
Obstetrical trauma, hysterectomy complications, scarring from episiotomy, radical cystectomy
3. Genital dysfunctions
Clitoral adhesions, vulvodynia
4. Endocrine/medical disorders
Diabetes mellitus, hypothalamo-pituitary disorders,
Sickle cell anaemia
Antidepressants, antipsychotics, antihypertensives, antiepileptics, alpha blockers, recreational drugs (chronic use)- heroin (& methadone), cocaine cancer chemotherapy 3,4-methyfenedioxymethamphatamine (MDMA or ecstacy)- orgasmic delay
Directed masturbation is used in a variety of contexts including group, individual, couples therapy, and bibliography. It is highly successful for treating primary anorgasmia.56
Extended foreplay and intromission did not enhance female coital response.57
Anxiety reduction techniques
The treatment originating from Masters and Johnson43 is their “sensate focus” that involves a graded (step-by-step), hierarchic sequence of body touching routed through nondemand genital touching by partner, guidance by female of genital manual and penile stimulation, and using coital positions to enhance pleasurable stimulation. Most studies now use this in combination with adjuvants such as sexual technique training, sex and communication education, bibliography, and pelvic exercises (Kegel exercises).
The concept that protracted foreplay and coitus will significantly increase the probability of the woman’s attaining coital orgasm is not substantiated by empirical data.53 Kegel reported that his pelvic exercises for prevention of stress incontinence appeared to improve the sexual pleasure and orgasms of the women who practiced them. Other studies, however, could not show this improvement (see Levin58 for brief review). Techniques for educating women about their anatomy and for enhancing communication skills have been effective in facilitating orgasmic ability.59
The coital alignment technique, a positional method (pelvic male override in the missionary position) to create stimulation of the clitoris during coital penile thrusting and thus enhance sexual arousal, is claimed to bring about female coital orgasm only if given the proper time to be learned and practiced correctly.60 It was found, however, to create more improvements in orgasmic ability than simply using directed masturbation.61
At present, no pharmacologic agent has been proven to be better than placebo in facilitating orgasmic function in women. Open-label trials without benefit of comparison with placebo often give false hopes. It is surprising how many researchers and investigators appear to forget that the human mind, given appropriate cues, is capable of either facilitating or inhibiting sexual arousal and orgasm. Meston et al. stress the importance of using a placebo based on the results of their study with ephedrine.9
An orgasm in the human female is a variable, transient peak sensation of intense pleasure creating an altered state of consciousness, usually with an initiation accompanied by involuntary, rhythmic contractions of the pelvic striated, circumvaginal musculature. There are often concomitant uterine and anal contractions and myotonia that resolve the sexually induced vasocongestion (sometimes only partially) and myotonia usually with an induction of well-being and contentment.62 More simply, while sexual arousal creates hyperemia and vaso- congestion in female pelvic structures, orgasms may be considered as the natural and pleasant means to ameliorate the pelvic discomfort. Clinically, orgasmic dysfunction is a common source of distress, and treatments require more evidence-based safety and efficacy data. More research is needed in the physiology of orgasm and the pathophysiology of orgasmic dysfunction in women.
1. Hollender MH. The need or wish to be held. Arch Gen Psychiatry 1970; 22; 445-53.
2. Schaefer LC. Women and Sex. London: Hutchinson, 1974.
3. Hite S. The Hite Report: A Nationwide Study of Female Sexuality. New York: Dell, 1976.
4. Lauman, EO, Gagnon JH, Michael RT et al. The Social Organisation of Sexuality: Sexual Practices in the United States. Chicago: University of Chicago, 1994.
5. Waterman CK, Chiauzzi EJ. The role of orgasm in male and female sexual enjoyment. JSxRei 1992: 18: 146-59.
6. Wellings K, Field, J, Johnson AM et al. Sexual Behaviour in Britain. London: Penguin Books, 1994.
7. Masters WH, Johnson VE. Human Sexual Response. Boston: Little, Brown, 1966.
8. Levin RJ. An orgasm is ... who defines what an orgasm is? Sex Relatsh Ther 2004; 19: 101-7.
9. Meston C, Hull E, Levin RJ, Sipski M. Women’s orgasm. In TF Lue, R Basson, R Rosen et al., eds. Sexual Medicine: Sexual Dysfunctions in Men and Women. Paris: Health Publications, 2004: 783-850.
10. Levin RJ. The female orgasm - a current appraisal. J Psychosom Res 1981; 25: 119-33.
11. Shainess N. Authentic feminine orgastic responses. In ET Adelson, ed. Sexuality and Psychoanalysis. New York: Brunner/Mazel, 1975: 145-60.
12. Fisher S. The Female Orgasm. New York: Basic Books, 1973.
13. Kinsey AC, Pomeroy WB, Martin C et al. Sexual Behaviour in the Human Female. Philadelphia: WB Saunders, 1953.
14. Ingelman-Sundberg A. The anterior vaginal wall as an organ for the transmission of active forces to the urethra and clitoris. Int Urogynecol J Pelvic Floor Dysfunct 1997; 8: 50-1.
15. Levin RJ. Is prolactin the biological “off-switch” for human sexual arousal? Sex Relatsh Ther 2003; 18: 282-7.
16. Levin RJ. Sexual desire and the deconstruction and reconstruction of the human female sexual response model of Masters and Johnson. In W Everaerd, E Laan & S Both, eds. Sexual Appetite, Desire and Motivation: Energetics of the Sexual System. Amsterdam: Royal Netherlands Academy of Arts and Science, 2001.
17. Singer I. The Goals of Human Sexuality. London: Wildwood House, 1973: pp 72-5.
18. Singer J, Singer I. Types of female orgasm. J Sex Res 1972; 8: 255-67.
19. Grimes DA. Role of the cervix in sexual response. Evidence for and against. Clin Obstet Gynecol 1999; 42: 972-8.
20. Ladas AK, Whipple B, Perry J. The G-Spot and Other Recent Discoveries About Human Sexuality. New York: Holt, Rinehart & E Winston, 1982: 149-51.
21. Bohlen G, Held JP, Sanderson MO et al. The female orgasm: pelvic contractions. Arch Sex Behav 1982; 11: 367-86.
22. Levin RJ, Wagner G. Orgasm in women in the laboratory - quantitative studies on duration, intensity, latency, and vaginal blood flow. Arch Sex Behav 1985; 14: 439-49.
23. Mah K, Binik YM. The nature of the human orgasm: a critical review of major trends. CUnPychglRev 2001; 21: 823-56.
24. Holstege GG, Geiorgiadis JR, Paans AM et al. Brain activation during human male ejaculation. J Neurosci 2003; 33: 9185-9.
25. Holstege GG. The central nervous system control of female orgasm. International Society for the Study of Women’s Sexual Health. Annual Meeting, Amsterdam, The Netherlands. 2003; Abstract, 179.
26. Whipple B, Komisaruk BR. Elevation of pain threshold by vaginal stimulation in women. Pain 1985; 21: 357-67.
27. Kaplan H. The New Sex Therapy: Active Treatment of Sexual Dysfunctions. New York: Brunner-Mazel, 1974.
28. Eysenck HJ, Wilson G. The Psychology of Sex. London: JM Dent, 1979.
29. Mead M. Male and Female. New York: William Morrow, 1949.
30. Levin RJ. Do women gain anything from coitus apart from pregnancy? Changes in the human female genital tract activated by coitus. J Sex Marital Ther 2003; 29: 59-69.
31. Kunz G, Beil D, Deininger H et al. The dynamics of rapid sperm transport through the female genital tract: evidence from vaginal sonography of uterine peristalsis and hysterosalpingoscintigraphy. Hum Reprod 1996; 11: 627-32.
32. Settlage DSF, Motoshima M, Tredway DR. Sperm transport from the external cervical os to the fallopian tube in women; a time and quantitation study. Fertil Steril 1973; 24: 655-61.
33. Levin RJ. Sex and the human female reproductive tract - what really happens during and after coitus. Int J Impot Res 1998; 10(Suppl 1): S14-S21.
34. Levin RJ. The physiology of sexual arousal in the human female: a recreational and procreational synthesis. Arch Sex Behav 2002; 31: 405-11.
35. Baker RR, Bellis MA. Human Sperm Competition, Copulation, Masturbation and Infidelity. London: Chapman & Hall, 1995.
36. Gerstenberg TC, Levin RJ, Wagner G. Erection and ejaculation in man. Assessment of the electromyographic activity of the bulbo- cavernosus and ischiocavernosus muscles. Br J Urol 1990; 65: 395-402.
37. Gould SJ, Lewontin RC. The spandrels of San Marco and the Panglossian paradigm: a critique of the adaptionist programme. Proc R Soc Lond B Biol Sci 1979; 205: 581-98.
38. Levin RJ. The mechanisms of human female sexual arousal. Annu Rev Sex Res 1992; 3: 1-48.
39. Passie T, Hartman U, Schneider U et al. On the function of groaning and hyperventilation during sexual intercourse: intensification of sexual experience by altering brain metabolism through hypocapnia. Med Hypotheses 2003; 60: 660-3.
40. Levin RJ, van Berlo W. Sexual arousal and orgasm in subjects who experience forced or non-consensual sexual stimulation - a review. j clim endocrinol metav 2004; 11: 82-8.
41. American Psychiatric Association. DSM-IV-TR: Diagnostic and Statistical Manual for Mental Disorders, 4th edn. Washington, DC: American Psychiatric Press, 2000.
42. World Health Organization. ICD-10 - International Classification of Diseases and Related Health Problems. Geneva: World Heath Organization, 1992.
43. Masters WH, Johnson VE. Human Sexual Inadequacy. Boston: Little, Brown, 1970.
44. Basson R, Berman J, Burnett A et al. Report of the International Consensus Development Conference on Female Sexual Dysfunction: Definitions and Classifications. Urology 2000; 163: 889-93.
45. Segraves RT. Editor’s comments. JmS^xMaritalT^er 2001; 27: 81.
46. Goldstein I, Graziottin A, Heiman JR et al. Female sexual dysfunction. In A Jardin, G Wagner, S Khoury et al., eds. Erectile Dysfunction. Plymouth: Plymbridge Distributors, 2000: 507-56.
47. Meston C. Validation of the female sexual function index (FSFI) in women with female orgasmic disorder and in women with hypoactive sexual desire disorder. J Sex Marital Ther 2003; 29: 39-46.
48. Basson R, Leiblum S, Brotto L et al. Definitions of women’s sexual dysfunction reconsidered: advocating expansion and revision. J Psychosom Obstet Gynaecol 2003; 24: 221-9.
49. Tiefer L. The medicalization of sexuality: conceptual, normative, and professional issues. Annu Rev Sex Res 1996; 7: 252-82.
50. Moynihan R. The making of a disease: female sexual dysfunction. BMJ 2003; 326: 45-7.
51. O’Gorman ERC. The treatment of frigidity: a comparative study of group and individual desensitization. Br J Psychiatry 1978; 132: 580-4.
52. Bancroft J, Loftus J, Scott Long J. Distress about sex: a national survey of women in heterosexual relationships. Arch Sex Behav 2003; 32: 193-208.
53. Heiman JR. Orgasmic disorders in women. In SR Leiblum, R Rosen, eds. Principles and Practices of Sex Therapy, 3rd edn. New York: Guilford Press, 2000.
54. Heiman JR, Meston CM. Empirically validated treatment for sexual dysfunction. Annu Rev Sex Res 1997; 8: 148-94.
55. Schover LR, Leiblum SR. Commentary: the stagnation of sex therapy. J Psychol Hum Sex 1994; 6: 5-30.
56. McMullen S, Rosen RC. Self-administered masturbation training in the treatment of primary orgasmic dysfunction. J Consult Clin Psychol 1979; 47: 912-18.
57. Huey CJ, Kline-Graber G, Graber B. Time factors and orgasmic response. Arch Sex Behav 1981; 10: 111-18.
58. Levin RJ. Measuring female genital functions- a research essential but still a clinical luxury. Sex Relat Ther 2004; 19: 191-200.
59. Everaaerd W, Dekker J. Treatment of secondary orgasmic dysfunction: a comparison of systematic desensitisation and sex therapy.__Behav ResT her 1982; 20: 269-74.
60. Pierce AP. The coital alignment technique (CAT): an overview of studies. j sex marital ther 2000; 26: 257-68.
61. Hurlbert DF, Apt C. The coital alignment technique and directed masturbation: a comparative study on female orgasm. J Sex Marital Ther 1995; 21: 21-9.