Cindy M. Meston, Bridget K. Freihart, & Amelia M. Stanton

The DSM-IV-TR included two sexual pain disorders, dyspareunia and vaginismus. The DSM-5 subworkgroup on sexual dysfunction combined these two disorders into genito-pelvic pain/penetration disorder. In DSM-IV-TR, dyspareunia was defined as genital and/or pelvic pain, while vaginismus referred to an involuntary spasm or tightening of the pelvic muscles. The merging of dyspareunia and vaginismus emphasizes the multidimensional nature of genital pain, particularly in women.

Genito-Pelvic Pain/Penetration Disorder
Definition, Diagnosis, and Prevalence

In the DSM-5, genito-pelvic pain/penetration disorder (GPPPD) is defined as persistent or recurrent difficulties with one or more of the following: (1) vaginal penetration during intercourse; (2) vulvovaginal or pelvic pain during vaginal intercourse or attempts at penetration; (3) fear or anxiety about vulvovaginal or pelvic pain in anticipation of, during, or as a result of vaginal penetration; and (4) tightening or tensing of the pelvic floor muscles during attempted vaginal penetration. To meet diagnostic criteria, at least one of these symptoms must have persisted for at least six months and must cause significant distress. The disorder can be specified by severity and as either lifetime or acquired.

GPPPD was created, in part, in response to arguments made by Binik (2010a), who questioned the logic of maintaining two separate sexual pain diagnoses for women, given the high rates of comorbidity between painful sex and difficulties with penetration. The overlap between these two concerns is notable, with one study finding that 72.4% of women with a diagnosis of vaginismus reported symptoms of dyspareunia, while 47.7% of women with a diagnosis of dyspareunia reported symptoms of vaginismus (Peixoto & Nobre, 2013).

There has also been some larger debate regarding the conceptualization of GPPPD, with some considering whether GPPPD should be considered a pain disorder that interferes with sexual activity or a sexual dysfunction characterized by pain (Kingsberg & Knudson, 2011). Evidence for the pain conceptualization comes from studies that suggest non-pelvic chronic pain is associated with chronic genito-pelvic pain (Paterson, Davis, Khalifé, Amsel, & Binik, 2009). While more research is needed, the DSM-5 subworkgroup decided to maintain the status of GPPPD as a sexual dysfunction.

In addition to the collapsing of dyspareunia and vaginismus, another important change with the release of DSM-5 is the exclusion of men from a sexual pain diagnosis. The DSM-IV- TR diagnosis of dyspareunia applied to both males and females. Due to a larger lack of empirical studies, male dyspareunia has been excluded from DSM-5’s diagnostic criteria for GPPPD (Bergeron, Rosen, & Pukall, 2014). There is, however, evidence to suggest that men do occasionally suffer from localized or generalized pain during sexual activity, with prevalence rates estimates between 5 and 15% (Clemons, 2005). To address this, researchers have coined the term “urological chronic pelvic pain syndrome” (UCPPS), which applies only to men but is not included in the DSM-5 (Shoskes, Nickel, Rackley, & Pontari, 2009). Davis and colleagues (2011) found that the patterns of sensitivity and pelvic floor muscle function observed in men with UCPPS are notably similar to those of women with GPPPD.

GPPPD is frequently comorbid with sexual arousal problems in women. The genital changes that occur during female genital arousal (i.e., swelling, lubrication of the genitals), facilitate penetrative intercourse. In absence of these cues to sexual readiness, intercourse can result in friction, tearing, and overstimulation of genital tissue leading to experiences of sexual pain. As a consequence, some have theorized that a lack of genital arousal may be a key antecedent to sexual pain symptoms.

GPPPD is new to DSM-5 and prevalence estimates are limited. One small Iranian sample yielded a prevalence rate of 10.5% among married women living in Tehran (Alizadeh et al, 2019). These rates may not, however, be generalizable at the population level. Prevalence estimates do exist for dyspareunia and vaginismus. Rates of dyspareunia range from 2-7% in general (Peixoto & Nobre, 2013), from 6.5-45% in older women (van Lankveld et al., 2010), and from 14-34% in younger women (van Lankveld et al., 2010). Prevalence rates for vaginismus are reported to be 5-6.6% (Fugl-Meyer et al., 2013; ter Kuile & Reissing, 2014). Notably, higher rates of painful sexual intercourse have been observed in clinical settings (Nobre & Pinto- Gouveia, 2008a) and in countries where arranged marriages, polygamy, and/or widow inheritance are common (Amidu et al., 2010; Yasan, Tamam, Ozkan, & Gurgen, 2009). Some women are at increased risk of genito-pelvic pain after giving birth (Rosen & Pukall, 2016), with 10% of women reporting post-partum genito-pelvic pain (Patterson et al, 2009). Additional risk factors for GPPPD include poor health, lower education, low family income, high stress, more frequent emotional problems, and the presence of urinary tract symptoms.

Factors Associated with Genito-Pelvic Pain/Penetration Disorder

Correlates of sexual pain in women include a number of medical conditions, as well as anxiety about sexual activity. When sex is painful, research suggests that women may develop anxiety related to sexuality that subsequently maintains the pain associated with GPPPD. Biological Factors

Genital pain is generally categorized as superficial or deep. Superficial pain may result from a dermatological disorder or other medical condition that impacts the genitalia (e.g., vaginal atrophy, anatomical variations, urinary tract infections, injury, and other diseases and infections of the vulva). Conversely, deep pain more commonly results from uterine fibroids, endometriosis, urinary disease, and ovarian disease (for review, see Schultz et al., 2005). Sexual pain has also been observed following treatment for cancer with pelvic radiation and chemotherapy (Fugl-Meyer et al., 2013; Kingsberg & Knudson, 2011).

At the superficial level, one of the major etiological factors for pain is a biological disorder known as provoked vestibulodynia (PVD; formerly vulvar vestibulitis syndrome). PVD is characterized by a sharp, burning pain experienced to any touch or pressure on the vulvar vestibule, a region that falls between the inner labia minora, the frenulum of the clitoris, and the lower portion of the vaginal opening (Pukall, Payne, Kao, Khalifé, & Binik, 2005). This condition can be diagnosed by a gynecologist by probing the area with a cotton swab to assess evoked pain sensations. PVD seems to be related to a history of yeast infections and hormonal events in adolescence, including the early onset of menstruation and use of oral contraceptives (Farmer et al., 2011; Pukall et al., 2005). Another potential cause of superficial genital pain is vulvovaginal atrophy, or the deterioration/reduction of flexibility and lubrication in vaginal tissue, naturally co-occuring with menopause. The vaginal symptoms reported by premenopausal women with PVD and postmenopausal women with vulvovaginal atrophy are markedly similar (Kao, Binik, Kapuscinski, & Khalifé, 2008).

One major hypothesized pathway to GPPPD involves the sensitization of neurons in the spinal cord and parts of the brain. More specifically, it has been theorized that intense stimulation of peripheral tissue during physical trauma or abrasive stimulation may sensitize

neurons that bring information about pain to receptive centers in the brain. As a result, the sensitized neurons will activate in response to less stimulation, or in some cases, in absence of simulation, resulting in pain from little to no touch. Indeed, women with this kind of genital pain also frequently report genital pain during nonsexual situations (Binik, 2010a).

Other etiological factors associated with deep genital pain include uterine fibroids, urinary diseases such as uterine retroversion and uterine myomas, ovarian diseases such as ovarian remnant syndrome, adenomyosis, endometriosis, pelvic congestion syndrome, levator ani musclae myalgia, and irritable bowel syndrome.

Little research has focused on the biological factors associated with vaginal spasms during sexual penetration. Some researchers have suggested that these involuntary spasms of the pelvic floor muscles may be due to genital malformations and/or poor general pelvic muscle control (ter Kuile & Reissing, 2014). As with genital pain, high rates of provoked PVD have been reported among women diagnosed with vaginal spasms (Binik, 2010b). Experts in sexual pain have suggested that the vaginal spasms may be a physiological response to intense pain during penetration; that is, the vaginal spasm could be the body’s automatic physical reaction to protect itself from anticipated pain.
Psychological Factors

Marked fear of pain and consequent anxiety with sexual activity have been proposed as both symptoms and etiological mechanisms for sexual pain. Women with genital pain exhibit a selective attentional bias towards pain stimuli as compared to controls, which is predicted by state and trait anxiety as well as fear of pain (Payne, Binik, Amsel, & Khalifé, 2005). Women with genital pain also tend to fear sexual interactions and show more phobic anxiety of sexual activity than sexually healthy women. It may be that after sexual pain has been experienced initially, anxiety about sexual activity maintains the pain by increasing hypervigilance toward pain cues. Evidence supports this pathway towards maintained pain—one study found that women with PVD displayed an attentional bias toward pain-related stimuli on an emotional stressor task when compared to matched control women without PVD (Payne et al., 2005). Unsurprisingly, women with sexual pain are also more likely to have negative attitudes towards sexuality than controls.

GPPPD is far more likely in women with histories of abuse. Indeed, one study found that women who experience sexual pain are 4.1 times more likely to have abuse histories (Harlow & Stewart, 2005). The experience of vaginal spasms has been associated with a history of abuse (Reissing, Binik, Khalifé, Cohen, & Amsel, 2004). Moreover, fear of physical abuse has been linked to genital pain (Landry & Bergeron, 2011).

Associations between depression and genital pain are frequently noted in the literature, while longitudinal studies have not observed a direct relationship (Schultz et al., 2005). It is feasible that women who are more depressed are more likely to attend to pain in general and sexual pain in particular, but there is no evidence at this point that depression is a causal factor underlying sexual pain or vice versa. It is more likely that this association is mediated by relationship satisfaction. Negative cognitions such as “My partner will leave me,” “I am a failure as a woman,” and “I must be tearing inside” are commonly reported by women with sexual pain. From a relational point of view, women with genital pain report more pain when their relational distress increases, an indication that sexual pain may be partially associated with negative feelings between partners. Consequently, more recent research has argued for the conceptualization of the GPPPD as a dyadic problem—one that is frequently maintained in the context of relationships, and one that must also be treated with relational factors in mind (Rosen & Bergeron, 2018).

With respect to vaginal spasms, women who experience vaginal spasms report high levels of anxiety symptoms. It is, however, unclear whether anxiety is a cause or consequence of such spasms (Schultz et al., 2005). Lower rates of positive attitudes toward one’s sexuality have been observed in women who experience spasms during sexual penetration (Reissing et al., 2004). It is possible that a lack of positive beliefs about one’s sexuality may create a negative feedback loop: discouraging a woman from seeking out and experiencing positive sexual interactions and contributing to avoidance of sexual activity.