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Modi ed from Lamont (1978) [15]
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However, as no consensus has been reached so far in unifying the two entities, they will be kept separate according to the latest classi cation [8]
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Prevalence
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Various degrees of dyspareunia are reported by 12 15% of coitally active women [11 13], and up to 453% of postmenopausal women [14] Vaginismus may occur in 05 1% of fertile women, although precise estimates are lacking [7] However, mild hyperactivity of the pelvic oor, that could coincide with grade I or II vaginismus, according to Lamont [15] (Table 251), may permit intercourse while causing coital pain [16,17]
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Pathophysiology
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Vaginal receptiveness is a prerequisite for intercourse, and requires anatomic and functional tissue integrity, both in resting and aroused states [16 19] Normal trophism, both mucosal and cutaneous, adequate hormonal impregnation, lack of in ammation, particularly at the introitus, normal tonicity of the perivaginal muscles, vascular, connective and neurologic integrity, and normal immune response are all considered necessary to guarantee vaginal habitability [6,7,15 17] Vaginal receptiveness
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may be further modulated by psychosexual, mental, and interpersonal factors, all of which may result in poor arousal with vaginal dryness [5,7,8 11] Fear of penetration, and a general muscular arousal secondary to anxiety, may cause a defensive contraction of the perivaginal muscles, leading to vaginismus [7,9,10] This disorder may also be the clinical correlate of a primary neurodystonia of the pelvic oor, as recently demonstrated with needle electromyography [20] It may be so severe as to completely prevent penetration [15,16] Vaginismus is the leading cause of unconsummated marriages in women Co-morbidity between life-long vaginismus and dyspareunia, and other FSD is frequently reported (Fig 251) The defensive pelvic oor contraction may also be secondary to genital pain, of whatever cause [21,22] Dyspareunia is the common symptom of a variety of coital pain-causing disorders (Table 252)
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25 palpation of the introital area (mostly at the 5 o clock and 7 o clock positions); (3) dyspareunia [23] From the pathophysiologic point of view, VV involves the upregulation of: (1) the immunologic system, ie of introital mast cells (with hyperproduction of both in ammatory molecules and nerve growth factors (NGF) [25 27]; (2) the pain system, with proliferation of local pain bers induced by the NGF [27 28], which may contribute to the hyperalgesia and allodynia, associated with neuropathic pain, reported by VV patients [2,3,6]; (3) hyperactivity of the levator ani, which can be antecedent to VV and comorbid with vaginismus of a mild degree [6,16,24], or secondary to the introital pain In either case, addressing the muscle component is a key part of the treatment [28 30] Hyperactivity of the pelvic oor may be triggered by non-genital, non-sexual causes, such as urologic factors (urge incontinence, when tightening the pelvic oor may be secondary to the aim of reinforcing the ability to control the bladder) [17], or anorectal problems (anismus, haemorrhoids, rhagades) [22] Medical ( organic ) factors, which are often under-evaluated in the clinical setting, may cause pain and they may combine with psychogenic (psychosexual) factors contributing to pain during intercourse They include hormonal/dystrophic, in ammatory, muscular, iatrogenic, neurologic and/or post-traumatic, vascular, connective, and immunologic causes [6,7,9 11,16 22,27] Co-morbidity with other sexual dysfunctions loss of desire, arousal disorders, orgasmic dif culties, and/or sexual pain related disorders is frequently reported with persisting or chronic dyspareunia [16] The second leading etiology of dyspareunia in the fertile age is postpartum pain associated with poor episiorraphy outcome and vaginal dryness secondary to the hypoestrogenic state when the woman is breastfeeding [31]
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Table 252 Etiology of dyspareunia: different causes may
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overlap or be associated with coital pain with complex and dynamic pathophysiologic interplay
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Biological Super cial/introital and/or mid-vaginal dyspareunia infectious: vulvitis, vulvar vestibulitis, vaginitis, cystitis in ammatory: with upregulation of mast cells hormonal: vulvovaginal atrophy anatomic: brous hymen, vaginal agenesis, Rokitansky syndrome muscular: primary or secondary hyperactivity of levator ani muscle iatrogenic: poor outcome of genital or perineal surgery; pelvic radiotherapy neurologic, inclusive of neuropathic pain connective and immunitary: Sj gren s syndrome vascular Deep dyspareunia endometriosis pelvic in ammatory disease (PID) pelvic varicocele chronic pelvic pain and referred pain outcome of pelvic or endovaginal radiotherapy abdominal cutaneous nerve entrapment syndrome (ACNES) Psychosexual co-morbidity with desire and/or arousal disorders, or vaginismus past sexual harassment and/or abuse affective disorders: depression and anxiety catastrophism as leading psychologic coping modality Context or couple related lack of emotional intimacy inadequate foreplay couple con icts; verbally, physically, or sexually abusive partner poor anatomic compatibility (penis size and/or infantile female genitalia) sexual dissatisfaction and consequent inadequate arousal Adapted from Graziottin (2003) [16]
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Vulvar vestibulitis (VV), a subset of vulvodynia, is its leading cause in women of fertile age [6,7,11,12,16,17,23,24] The diagnostic triad is: (1) severe pain upon vestibular touch or attempted vaginal entry; (2) exquisite tenderness to cotton-swab
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