More than 15 years have passed since the approval and subsequent widespread availability of the oral treatments for male sexual dysfunction (e.g., sildenafil, vardenafil, and tadalafil); as a result, research exploring the pathophysiology, epidemiology, assessment, and treatment of sexual dysfunctions has had an unprecedented surge. Methodological sophistication has soared, particularly in the area of neural imaging for low desire and genetic studies of orgasmic dysfunction and dyspareunia. With the publication of the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5; APA, 2013) and the upcoming 11th edition of the International Classification of Diseases (ICD-11) (forthcoming), there has also been an intensified examination of the reliability and validity of these categories of sexual disorders.

Unlike their division in the DSM-IV-TR (APA, 2000), which categorized the sexual dysfunctions according to which phase of Masters and Johnson’s four-stage human sexual response cycle (Masters & Johnson, 1966) was disrupted, the DSM-5 has abandoned this model of linear sexual response. This change was the result of long-standing dissatisfaction with its ability to account for the variability in sexual response across individuals. In brief, the sexual dysfunctions in previous editions of the DSM were separated into disorders of desire, arousal, and orgasm (and pain), which fit with Masters and Johnson’s linear conceptualization of the human sexual response cycle—that is, in linear stages from sexual desire to arousal to orgasm. As has been noted (e.g., Binik, 2005, 2010a, 2010b), the sexual pain disorders were added as a fourth category of sexual dysfunction although “pain” was not considered to be part of the human sexual response cycle. This four-category system of diagnosing sexual dysfunctions has been commonplace since DSM-III in 1980. However, given numerous criticisms about this linear response cycle, particularly when conceptualizing women’s sexual problems, over the past decade there have been concerted efforts to redefine these categories. In particular, concerns about the lack of generalizability of the sexual response cycle for women were that (a) it is based on the sexual response patterns of men; (b) it assumes a linear progression of sexual experience from desire to arousal to orgasm, although healthy sexual experiences can progress in any order and do not need to proceed in this sequence for satisfaction to occur; (c) many of the experiences that are considered normal parts of female sexual response (e.g., fantasizing) are not reported in all women; and (d) characteristics of the sample on which the human sexual response cycle were based are considered biased (Hill & Preston, 1996; Klusmann, 2002; Regan & Berscheid, 1996). One of the alternative classifications that were proposed emerged from an international group of academic clinicians in sexual medicine who were sponsored by the American Foundation for Urologic Diseases to form a consensus panel (Basson et al., 2003). Interestingly, despite the group’s criticism about the DSM-IV-TR categories of sexual dysfunction, they retained the overall structure and made minor revisions to the diagnostic criteria of the disorders without any attempt made to overhaul the existing nosology.

Another system for classifying sexual dysfunctions as “problems” was proposed by the New View Task Force, led by sexologist Leonore Tiefer. The resulting “New View Document” (Kaschak & Tiefer, 2002; Tiefer, 2001) was a radical departure from the DSM classification system and suggested that sexual problems in women have been overdiagnosed and medicalized, and the designating of “dysfunctions” was found to be highly problematic. This alternate system focused on causes instead of symptoms and concluded that such difficulties can be a result of sociocultural, political, or economic factors; partner and relationship status; psychological factors; or medical factors. The New View nosology fervently rejected the biological emphasis of sexual complaints that was inherent in the DSM, and the associated “medicalization of sex” that resulted. Empirical support for the New View system is sparse; however, some data suggest the usefulness of this classification scheme in that 98% of the sexual issues in one sample of British women could be classified using the New View framework (Nicholls, 2008).

In the absence of a universally agreed upon underlying model of sexual response, the sexual dysfunctions in DSM-5 are listed in alphabetical order. This represents a radical departure from past DSMs and has generated some controversy (Balon & Clayton, 2014). Collectively, sexual dysfunctions are defined by the DSM-5 as “a heterogeneous group of disorders that are typically characterized by a clinically significant disturbance in a person’s ability to respond sexually or to experience sexual pleasure” (APA, 2013, p. 497). The definition also emphasizes the need for the clinician to exercise clinical judgment when deciding if the difficulty is due to lack of adequate sexual stimulation, in which case a diagnosis of a mental illness is clearly not appropriate.

The DSM-5 (APA, 2013) list of sexual dysfunctions includes: delayed ejaculation, erectile disorder, female orgasmic disorder, female sexual interest/arousal disorder, genito-pelvic pain/penetration disorder, male hypoactive sexual desire disorder, premature (early) ejaculation, substance/medication-induced sexual dysfunction, other specified sexual dysfunction, and unspecified sexual dysfunction. Like previous editions of the DSM, each sexual dysfunction in the DSM-5 can be specified as being either lifelong (i.e., the problem has existed since the individual first became sexually active) or acquired (i.e., the problem is new in onset); and generalized (i.e., the problem is not limited to certain types of stimulation, situations, or partners) or situational (i.e., the problem occurs only with select types of stimulation, situations, or partners). The DSM-5 also has a new severity specifier in which the clinician is asked to rate the level of distress as either mild, moderate, or severe.

Also new to DSM-5 is a list of five associated features that the clinician should be mindful of during assessment. These are features that may play a role in etiology and/or maintenance of the sexual difficulty and include: (1) partner factors (e.g., a partner’s sexual dysfunction), (2) relationship factors (e.g., problematic communication patterns), (3) individual vulnerability factors (e.g., depression or other associated psychopathology), (4) cultural/religious factors (e.g., attitudinal prohibitions against sex), (5) medical factors (e.g., chronic pain or fatigue). During assessment, the clinician is asked to assess each of these domains, taking into account the extent to which each may account for the current presenting complaint. These issues then may be addressed in the course of managing the sexual difficulty.

Whereas criterion A for each of the sexual dysfunctions outlines the diagnostic criteria, criterion B for each delineates the duration criterion in that symptoms must be present for a minimum duration of at least 6 months. The addition of this criterion to DSM-5 is intended to reduce the probability that temporary or otherwise adaptive changes in sexual functioning may be diagnosed as a sexual dysfunction. Also required for a diagnosis across the sexual dysfunctions is the presence of clinically significant distress in the individual (criterion C).

The range of factors that would exclude the diagnosis of a sexual dysfunction has also been expanded from previous editions of the DSM. For example, in addition to the rule-outs due to the presence of another psychiatric disorder, a medication, or a medical condition that completely accounts for the presenting sexual problems, a diagnosis of sexual dysfunction is not made if the symptoms are the result of severe relationship distress (such as domestic violence) or significant stressors.

Primary care providers are often the first point of contact for individuals with sexual concerns. Adequate assessment requires a thorough biopsychosocial approach, including attention to early family history, relationship and sexual history, and psychiatric status and history, and may require the assistance of a sexual health expert. In some cases, preexisting and confounding contributors may be directly responsible for the sexual issues. For example, relationship factors can mask as sexual dysfunction, as these constructs are highly correlated (e.g., Dennerstein, Lehert, Guthrie, & Burger, 2007). Problems in the relationship can directly impact sexual functioning, and difficulties expressing one’s sexual needs can negatively impact sexual desire. In general, men have more difficulty than women with discussing emotional and sexual issues (Banmen & Vogel, 1985). It is important to note that some decline in sexual function is normative with age and relationship duration (Klusmann, 2002) and should not be considered a sexual dysfunction. Cases in which lack of adequate sexual stimulation accounts for the sexual problems should not be diagnosed as a dysfunction. The clinician is advised to take into account factors that affect sexual function, such as age, novelty of the sexual partner or situation, and recent frequency of sexual activity, before making a sexual diagnosis.

Sometimes a sexual difficulty may be an adaptive reaction to a stressful or aversive situation. For example, in homosexuals who are ashamed or insecure about their sexual orientation and who are, thus, in heterosexual relationships, sexual desire may be low in response to individuals of the opposite sex but may be satisfactory toward individuals of the desired sex (Sandfort & de Keizer, 2001). In this case, a diagnosis of sexual desire disorder would not be warranted. The list of associated features for each sexual dysfunction allows a clinician to determine whether individual vulnerability factors, including stress, are contributing to the sexual complaints. This would orient treatment to the stressor and may reduce the likelihood of prematurely resorting to pharmacological aids.

In the past decade, there have been several international surveys aimed at determining the prevalence of sexual difficulties. The National Health and Social Life Survey (NHSLS), a population-based study of 3,159 American men and women between the ages of 18 and 59 (Laumann, Gagnon, Michael, & Michaels, 1994), had an excellent response rate (79%) and used a combination of face-to-face interviews and questionnaires. The authors inquired about (a) lack of sexual desire, (b) arousal difficulties, (c) problems achieving climax or ejaculation, (d) anxiety about sexual performance, (e) climaxing or ejaculating too quickly, (f) pain during intercourse, and (g) not finding sex pleasurable. The NHSLS found a total prevalence for sexual difficulties of 43% in women and 31% in men (Laumann, Paik, & Rosen, 1999), although these figures may be inflated because the study did not inquire about distress arising from sexual complaints.

A thorough biopsychosocial interview is considered foundational in the assessment of sexual difficulties. An important aspect in assessing sexual dysfunction is determining whether the problem is related to a psychological versus a biological/organic etiology or both. It is also important for the clinician to distinguish lifelong (primary) versus acquired (secondary) and generalized versus situational difficulties as these may point to important etiological factors. For example, clinicians should inquire about morning erections to gain a sense of the degree to which ED is situational or generalized. Complete loss of morning erections suggests a vascular or neurological component to the ED, and a referral to a qualified urologist is indicated.

Assessment involves face-to-face interviews of the presenting person, ideally together with and separately from the partner, covering known and supposed predisposing, precipitating, and perpetuating issues relevant to the sexual difficulty. These include assessments of mood and general psychiatric status, medications and medical comorbidities, psychosexual history, and personal history. Although many self-report questionnaires are available, none can replace a thorough clinical interview (Brotto, Bitzer, Laan, Leiblum, & Luria, 2010).

Accurate assessment of medical factors often requires physical and laboratory examinations. In men, testosterone that is free, bound to albumin, and bound to SHBG should be measured first thing in the morning. A thorough assessment of sexual interest/arousal disorder in women involves separately assessing for difficulties in mental sexual arousal and interest versus genital excitement. Assessment of GPPPD may include a physical examination of the level of voluntary control of the pelvic floor muscles, pelvic floor muscle tonus, presence of vaginal wall prolapse, signs of vaginal atrophy, size of introitus, presence of discharge, evidence of infection (acute or chronic), epithelial disorders, and/or pain by a qualified health professional (usually a gynecologist or primary care provider with specialized training in vulvovaginal disorders).

To assess for the criterion of marked vulvovaginal pain when making a diagnosis of GPPPD, the physician often uses the cotton swab test in which the vestibule is palpated with a cotton swab and the woman reports areas of particular tenderness or pain. In addition to pain and tenderness upon touch, there is erythema (redness) in the area of the vestibule (Friedrich, 1987). During such an assessment, it is important for the clinician to elicit as much information as possible regarding the qualities of pain (location, intensity, characteristics). Because the elicitation of pain may evoke distressing emotions for the woman, it is important for the clinician to be sensitive to the woman’s emotional state and only conduct the genital exam if sufficient explanation and preparation has been given. Since pelvic floor muscle spasms have been found to be an unreliable indicator of GPPPD, the diagnosis is largely based on the patient’s self-report of difficulties with intercourse, including anticipation of pain, anxiety, and phobic avoidance.

Assessment of PE in clinical trials has adopted the stop-watch technique in which the duration of time between penetration and ejaculation is monitored, usually by the man’s partner. Studies using this methodology have led to the current recommendation that one minute be used as the threshold for determining when early ejaculation might constitute a sexual dysfunction. However, this additional layer of performance anxiety may artificially inflate the man’s dysfunction, leaving this technique suboptimal, particularly when making a diagnosis of PE. Accurate assessment can also be confounded by embarrassment (Symonds et al., 2003). Grenier and Byers (2001) found marked differences in the prevalence of PE depending on the operational definition of “rapid.” They concluded that a multifaceted approach should include assessment of behavior, affect, self-efficacy, and the degree of severity of different dimensions of PE.

As implied in the previous section on assessment, all the sexual dysfunctions are considered to be biopsychosocial in their etiology. Although previous editions of the DSM included the specifier of “due to psychological factors” or “due to combined factors,” this has been eliminated from the DSM-5 due to the recognition that this level of delineation is rarely possible. Even in cases when there is a clear biological or medical etiology to the sexual symptoms, sexual functioning typically involves an integration of all organ systems of the body, the vascular system, muscles, and the brain, making multifactorial etiology the norm rather than the exception.

Low desire in both men and women is considered to result from a combination of organic and psychological factors. In women, relationship duration, age, feelings for one’s partner, and depression have all been associated with sexual desire disorder (Brotto et al., 2010). In fact, 27% to 62% of women with low desire also meet criteria for a depressive disorder (Hartmann, Heiser, Ruffer-Hesse, & Kloth, 2002; Phillips & Slaughter, 2000). Interestingly, a few studies report that depressed mood is associated with increased frequency of masturbation (Cyranowski et al., 2004; Frolich & Meston, 2002)—one potential index of sexual desire. Low testosterone and testosterone metabolites have not been found to significantly differentiate women with and without HSDD, although the latter are found to have lower levels of the androgen precursor, dihydroepiandrosterone (DHEA; Basson, Brotto, Petkau, & Labrie, 2010). Women with HSDD show different patterns of neural activation particularly in neural circuits involved with encoding arousing stimuli, retrieval of past erotic situations, or both (Arnow et al., 2009).

Recent studies on cultural influences in low desire have shown women from East Asian heritage to have lower levels of desire compared to women from European descent. Moreover, among the East Asian women, those with higher levels of mainstream (i.e., Westernized) acculturation had higher sexual desire than those who retained their culture or heritage (Woo, Brotto, & Gorzalka, 2011). The variable “sex guilt,” or “a generalized expectancy for self-mediated punishment for violating or for anticipating violating standards of proper sexual conduct,” has been shown to mediate the relationship between culture and sexual desire in women. Therefore, sex guilt may be a future treatment target among ethnic minority women presenting with sexual desire complaints (Woo et al., 2011).

Androgen deprivation and hyperprolactinemia seem to play a more pertinent role in HSDD in men (Brotto, 2010b). Hyperprolactinemia may result from antipsychotic medications or prolactin-secreting tumors. With respect to androgen deprivation, as men age, sex hormone binding globulin (SHBG) levels increase, thereby decreasing the level of free testosterone. Similarly, bioavailable testosterone begins to decline when men are in their 30s and 40s, and continues to decline throughout the life span (Seidman, 2003). A syndrome known as androgen deficiency in the aging male (ADAM) or partial ADAM (PADAM) can include fatigue, depression, reduced sex drive, erectile disorder, and changes in mood and cognition (Morales, Heaton, & Carson, 2000). There is significant comorbidity between ED and HSDD in men such that men experiencing erectile difficulties eventually have reduced levels of desire.

In men, hypothyroidism, hypogonadism, and hyperprolactinemia are also associated with ED (Morales et al., 2004). Radical genital or pelvic surgeries can result in a sudden loss of erectile function, such as the case with prostate cancer surgery (Bolt, Evans, & Marshall, 1987; Stanford et al., 2000), especially if the procedure did not involve nerve-sparing techniques. Among men treated for diabetes, the prevalence of ED is 28% (Feldman, Goldstein, Hatzichristou, Krane, & McKinlay, 1994). Overall, any medical condition that causes blood vessel damage will likely negatively impact erectile function. Although often presumed to have an exclusive organic etiology, it is suspected that there are many cases of ED where psychological factors are responsible but go unrecognized. For example, major depressive disorder has been strongly associated with ED (Araujo, Durante, Feldman, Goldstein, & McKinley, 1998). Distinguishing ED that is secondary to the depression itself versus as a result of antidepressant use (Ferguson, 2001) is an important consideration.

Performance anxiety is also strongly associated with erectile dysfunction. Anxiety or stress may activate the sympathetic nervous system, which can both increase smooth muscle tone and interfere with signals from the sacral spinal cord. The man with no prior history of ED who fails to reach an erection one time due to stress or other factors may become concerned about his future erectile ability such that his ED is maintained by performance anxiety. Implicit in this example is the phenomenon that factors that maintain a sexual dysfunction may not be the same factors that initially triggered the complaint.

In the case of women, vaginal photoplethysmography as a measure of genital vagocongestion has not been able to differentiate women with from those without significant sexual arousal concerns (Laan, van Driel, & van Lunsen, 2008). For this reason, it is assumed that impairments in genital blood flow do not underlie genital arousal complaints of women. The reasons for women’s lack of awareness of their genital responding, otherwise known as desynchrony (or lack of concordance), compared to men (Chivers, Seto, Lalumiere, Laan, & Grimbos, 2010) has become the focus of study because it may shed light on different models of sexual responding between the sexes.

The precise etiology of PE is unknown, but a combination of psychological, biological, and behavioral components likely contribute. Much of the research exploring etiology in PE is based on rodent studies in which serotonergic disruption is the primary etiological factor. Stimulation of 5-HT_1A receptors in rats leads to rapid ejaculation, whereas hyposensitivity at the 5-HT_2C receptor shortens ejaculation time (Waldinger, 2002). Studies in rodents have led Waldinger, a leading authority on PE, to formulate the Ejaculation Threshold Hypothesis, which posits that men with PE have a lower ejaculatory setpoint (threshold) due to low serotonin neurotransmission, leading them to tolerate only a very low amount of sexual arousal prior to ejaculation (Waldinger, 2005). There is also evidence of a genetic predisposition to PE given the finding that 71% of first-degree relatives of men with PE also have the condition (Waldinger, Rietschel, Nothen, Hengeveld, & Olivier, 1998).

Acquired and/or situational PE may suggest a more psychological etiology related to early sexual experiences, low frequency of sexual activity, or poor ejaculatory control techniques. Among men with PE, 50% of the female partners meet criteria for anorgasmia and 54% meet criteria for hypoactive sexual desire (Fugl-Meyer & Sjogren Fugl-Meyer, 1999), suggesting a reciprocal relationship between PE and women’s sexual complaints. Masters and Johnson (1970) forwarded the possibility that performance anxiety leads to loss of ejaculatory control, but more recent research does not support the role for anxiety in PE in the clinical or the laboratory setting (Strassberg, Kelly, Carroll, & Kircher, 1987). Instead, high anxiety, if present, may be the consequence, rather than the cause, of PE.

Waldinger (2005) has speculated that organic factors related to genetics have a likely role in etiology. In particular, aberrations in the serotonergic system, such as hyperactivity at the 5-HT_2C receptor and hypoactivity at the 5-HT_1A receptor, have been found in rodent studies to be related to delayed ejaculation. Androgen deficiency with aging and/or hypogonadism is also linked to Delayed Ejaculation, as are age and prostate disease (Laumann et al., 2005). Injury to the lumbar sympathetic ganglia (i.e., such as from multiple sclerosis) may also delay ejaculation. One chart review has suggested that idiosyncratic masturbatory style (e.g., using rapid stimulation or pressure in a manner that is not easily duplicated by partnered sexual activity), as well as using a variant sexual fantasy (e.g., fantasy about S&M), act as predisposing factors for delayed ejaculation (Perelman, 2006).

The same organic factors implicated in delayed ejaculation in men have been associated with FOD in women (e.g., neurologic injury, SSRI use, alcohol). There may also be a genetic aspect to orgasmic difficulties in women given the finding of higher correlations between orgasmic frequency during masturbation and orgasmic frequency during sexual intercourse in monozygotic twins compared to dizygotic twins (Dunne et al., 1997). In addition, the heritability for orgasm problems with intercourse is 31% to 34%, and the rate for orgasm problems in masturbation is 37% to 45% (Dunn, Cherkas, & Spector, 2005).

Psychological factors found to be associated with anorgasmia in women include lower educational levels, high religiosity, sex guilt (Laumann et al., 1999), and a dim outlook for the future (Laumann et al., 2005). Although sexual abuse has been associated with anorgasmia in some studies, other studies have failed to find such a relationship. There does not appear to be a correlation between relationship satisfaction and orgasmic ability, given that many women are sexually satisfied with their partners despite not consistently or, perhaps, ever attaining orgasm with intercourse (Basson, 2004).

Pelvic or vulvar surgeries, chemotherapy, or radiation have all been associated with dyspareunia (Amsterdam, Carter, & Krychman, 2006), as have menopausal changes due to loss of estrogen and subsequent loss of elasticity in the vaginal tissues. In one type of genital pain, provoked vestibulodynia (PVD), biological etiological factors have included yeast infections, use of oral contraceptives, early menarche, a genetic predisposition, human papillomavirus, and urethral conditions or infections (Pukall, Payne, Kao, Khalifé, & Binik, 2005; Pukall, Strigo, et al., 2005). Assessment with functional magnetic resonance imaging (fMRI) indicates that women with PVD have a more general hypersensitivity to touch and pain compared to unaffected women (Pukall, Strigo, et al., 2005).

Although psychological factors are not considered primary in GPPPD, personality and psychiatric symptoms can exacerbate pain as well as pain-induced affect. Among the many psychological factors correlated with genital pain are anxiety, depression, low self-esteem, harm avoidance, somatization, shyness, and pain catastrophization (as summarized in Pukall, Payne, et al., 2005).

With regard to the pelvic floor muscle contractions that characterize GPPPD, Weijmar Schultz and Van de Wiel (2005) summarize eight major theories of etiology. Although these researchers focused on the DSM-IV-TR category of vaginismus, one could easily apply their findings to GPPPD. One theory is a behavioral view in which a conditioned anxiety reaction results in vaginal muscle spasm. This conditioning may have taken place during one episode of learning (e.g., as in the case of sexual assault with forced penetration) or over repeated trials (e.g., as in the case of voluntary intercourse in a woman with dyspareunia). The fear of pain from intercourse and the subsequent avoidance of any genital contact maintains the phobic anxiety.

According to the overactive pelvic floor muscle view (Weijmar Schultz & van de Wiel, 2005), some have regarded the pelvic floor muscle symptoms of GPPPD as a pelvic floor dysfunction and not as a sexual dysfunction. Because conditioning is the likely mechanism behind the overactive pelvic floor muscles, physiotherapy with biofeedback is the most logical treatment approach (Rosenbaum, 2003).

The interactional view (Weijmar Schultz & van de Wiel, 2005) suggests that pelvic floor hypertonus maintains balance between partners. Although research on this view is sparse, it is not uncommon in the clinical setting for male partners to be passive, dependent, anxious, and lacking in self-confidence. There is also evidence that these partners suffer from sexual dysfunction themselves (Lamont, 1978); therefore, GPPPD may function to maintain balance in the sexless relationship.

As implied in the section on etiology, there has been a pendulum shift in the past decade and a half, with much research attention focused on finding effective pharmacological treatments for the most prevalent sexual complaints (low desire in women, erectile and ejaculation difficulties in men). As a result, there has been a recent dearth of randomized controlled trials of psychological treatments, and much of the information on efficacy of psychological treatments is based on studies conducted in the 1970s and 1980s. However, psychological treatments are effective and needed (Heiman, 2002).

Treatment for HSDD largely depends on the presumed etiology and can involve any combination of psychotherapy (either alone or with the partner), medications, or hormonal therapy. Psychological therapy may involve exploration of couple issues, including anger, trust, exploration of an affair, and feelings of attractiveness. Treatment may also encourage the use of fantasies, erotic stimuli, and other forms of sexual activity besides intercourse. Unfortunately, there are no controlled publications on the efficacy of psychological treatment without concomitant medication treatment for HSDD in men.

Among the pharmacological treatments for low desire, bupropion (marketed as the antidepressant Wellbutrin) is a norepinephrine and dopamine agonist that has been found to have an efficacy rate of approximately 86% in nondepressed men with HSDD (Crenshaw, Goldberg, & Stern, 1987). Testosterone replacement has been the primary hormonal treatment studied for men with HSDD and is administered as an injection, a patch, or a gel. In a recent meta-analysis of the effects of testosterone on sexual dysfunction in men with heterogeneous sexual complaints, testosterone treatment improved sexual desire among men with clinically low levels of testosterone but not in men with normal levels (Isidori et al., 2005).