GenitoPelvic Pain/Penetration Disorder

1. GenitoPelvic Pain/Penetration Disorder t-eftekhartums

2. Genito-Pelvic Pain/Penetration Disorder • Diagnosis Statistical Manual of Mental Disorders (DSM-5; American Psychiatric Association, 2013) dyspareunia and vaginismus were typically classified as distinct sexual pain disorders. • This new classification unifies vaginismus and dyspareunia into one category called • “genito-pelvic pain/penetration disorder” due to the clinical difficulties to distinguishing these condition

3. DSM-5 Diagnostic Criteriafor Genito-Pelvic Pain/ Penetration Disorder • A. Persistent or recurrent difficulties with one (or more) of the following: 1. Vaginal penetration during intercourse. • 2. Marked vulvo vaginal or pelvic pain during vaginal intercourse orpenetration attempts. • 3. Marked fear or anxiety about vulvovaginal or pelvic pain inanticipation of, during, or as a result of vaginal penetration. • 4. Marked tensing or tightening of the pelvic floor muscles duringattempted vaginal penetration. .

4. DSM-5 Diagnostic Criteria for Genito-Pelvic Pain/ Penetration Disorder : B. The symptoms in Criterion A- have persisted for a minimum duration of approximately 6 months. C-. The symptoms in Criterion A cause clinically significant distress in the individual. D-. The sexual dysfunction is not better explained by a nonsexual mental disorder or as a consequence of a severe relationship distress (e.g., partner violence) or other significant stressors and is not attribute table to the effects of a substance/medication or another medical condition

6. Opposite to this wrong belief, • pain is rarely purely psychogenic,and coitalpain/dyspareunia is no exception. • Like all pain syndromes, it usually has one or more biological etiologicfactors • that can be differentiated according to the woman’shormonal status and the site of pain. • The etiology ofdyspareunia is complex

7. Sexual pain disorders can therefore be considered as • multifactorial, multisystemic, complex : - Multifactorial: • biological, psychosexual, relational factorscan coexist in a woman complaining of coital pain. • Over time, these different factors may • act as predisposing,precipitating, or perpetuating sexual pain disorders.

8. Multisystemic: sexual function involves • nervous, • endocrine, • vascular, • immunological systems • vaginal ecosystem • these variousbiological systems

9. Complex:. • coital pain is greater than the simple peripheral tissue damage that may initially trigger the nociceptive component • When GPPPD becomes chronic, the pathophysiology of pain may gradually shift from nociceptive, a friend signal that should induce self protection and defense, to neuropathic, with a progressive involvement of the CNS

10. Vulvodynia • chronic painin the vulvar area of at least 3–6 M duration. • This comprehensiveword includes • heterogeneous vulvar conditions • different etiologies,pathophysiologies, • commonsymptom: an invalidating,chronic vulvar pain.

12. (A) ilioinguina ln(L1) • ; (B) genitofemoraln (L1-2); and • (C, D) branches of the pudendaln (S2-4). • (C) the dorsal nerve of the clitoris (shown deeper as dashed lines in muscles of the urogenital diaphragm) • , (D) the perineal nerve, which innervates the labia majora and perinuem, • (E) the inferior rectal nerve, which innervates the perianal area. The pudendalnerve also innervates the external anal sphincter and deep muscles of the urogenital • The triangle

13. Dyspareunia;defines the persistent or recurrent pain withattempted or complete vaginal entry and/or penile vaginalintercourse • Vaginismus;persistent or recurrentdifficultiesof the woman to allow vaginal entry of a penis, a finger,and/or any object, despite the woman’s expressed wish to doso.There is often (phobic) avoidance and • anticipation/fear/experience of pain, along with • variable involuntary pelvicmuscle contraction). • Structural or other physicalabnormalities must be ruled out/addressed.

14. Vaginal receptiveness may be further modulatedby; psychosexual, mental, interpersonal factors may result in poor arousal with vaginal dryness .Fear of penetration general muscular arousal secondaryto anxiety, defensive contraction of theperivaginal muscles, leading to lifelong vaginismus.

15. Severity of vaginismus (grades) • I Spasm of the levatorani, that disappears with patient’s reassurance • II Spasm of the levatorani, that persists during the gynecologic examination • III Spasm of the levatorani and buttock’s tension at any tentative of gynecologic examination IV Mild neurovegetative arousal, spasm of the elevator, dorsal arching, thighs adduction, defense and retraction V- Extreme defense and neurovegetative arousal, with refusal of the gynecologic examination

18. women with vulvodynia weresignificantly more likely to report chronic medical conditions,; • interstitial cystitis(BPS/IC) • fibromyalgia • IBS • diagnosed IC,more than half (51.4%) were diagnosed with vulvodynia

19. B. Vulvodynia • 1. Generalized • (a) Provoked (sexual, nonsexual, or both) • (b) Unprovoked • (c) Mixed (provoked and unprovoked) • 2. Localized (vestibulodynia, clitorodynia, hemi vulvodynia, etc.) • (a) Provoked (sexual, nonsexual, or both) • (b) Unprovoked • (c) Mixed (provoked and unprovoked)

20. Biological Correlates of Pain • prominent and more frequent • biological correlate of pain is inflammation. • In case of GPPPD, inflammationis histologically documented at genital, vestibular andvaginal sites, and in other organs (bladder, colon, pelvis, …)when an important comorbidity is reported.

21. Mast cells, defined as the powerful director of the inflammatoryorchestra, are the single biological agents that bridgeinflammation to pain. The mast cell can be activated by ainfections, • estrogens fluctuations • which trigger flares of pain during periods, • chemical and physical noxae, • menstrual blood when releasedin the tissues (outside the uterus) as it happens in endometriosis, • the mechanical trauma of intercourse in case of vaginaldryness, introital pain, hyperactive pelvic floor withvaginismus

22. Mast cells are the main source of inflammatory mediators. • These peripheral cell types are located in the dermisadjacentto • blood vessels, • nerve endings • glandular ducts • have a cytoplasm filled with spherical granules.

23. Mast cells’ granules contain many factors implicated in neurogenic inflammation like NGF, tumor necrosis factor (TNF), protease, and cytokines .

25. Physical, chemical and mechanical stimuli activate local mast cells causing degranulation and secretion of mediators which have been found to sensitize and induce the proliferationof C-afferent nerve fibers

26. Nociceptors are classified; • Aδ, which are small diameter,lightly myelinated, • C-fibers, which are not myelinated. • The nociceptors neurons pass in the peripheral nervesand enter the spinal cord at the dermatomal level ascribed by • their insertion.

27. Vulvodynia can trigger dyspareunia, and a painful intercoursemay worsen or precipitate vulvar pain, and concur tomaintain it. • A lifelong hyperactive pelvic floor (“myogenic • hyperactivity,” associated or not with phobia of penetration)anatomically reduces the entrance of the vagina. • This predisposesthe introital vestibular mucosa to microabrasionsmechanically provoked by any attempt of intercourse

28. 1. the mast cell is hyperactivated, with hyperproduction ofinflammatory molecules andneurotrophins such as the;Nerve Growth Factor (NGF), which induces: • 2. the proliferation of pain nerve fibers, responsible forthe introitalhyperalgesia, and allodynia, and induces orworsen: • 3. the hyperactivity of the pelvic floor

29. Physical, chemical and mechanical stimuli • recurrent/chronic inflammation of theintroital mucosa,(from Candida,Herpes, Gardnerella) • physical damages (laser therapydiatermo coagulation) • chemical irritation(fromsoaps, perfumes, douche gel, or other substances) allergies

30. neuropathic pain isexpressed by two abnormal sensory processes: • hyperalgesiaand/or allodynia. • Hyperalgesia is defined as an increased • response to a stimulus that is normally painful • allodyniaas pain due to a stimulus that is not normally painful

31. a chronic inflammatory process involving different pelvic organs. • Themast cell is a travelling cell, patrolling all the body andspecifically theboundaries such as • colonic mucosa, bladder mucosa vestibulararea: • this may helpto understand comorbidities among organs and systemlocated in different sites the involvement of nerves innervating organs in close • proximity (e.g., the pudendal nerve): the term of cross-talk • has been used to express this process of “sharing pain.”

32. every time a woman complains of painfulintercourse, always actively investigate if she suffers as wellof • : postcoital cystitis (24–72 h after intercourse), • BPS/IC • vestibular/vaginal burning • IBS, CPP, • fibromyalgia • headache.

33. Vulvodynia and comorbidities 50% of persons with IBS syndrome had IC 38% of patients with IC had IBS syndrome 26% of those with IC had vulvodynia

34. Impact of Vulvodyniaon Physicaland Psychosexual Health • unwanted pain is the strongest reflex • inhibitor of desireofmental and physical arousalwith low desire, vaginal dryness • aprogressive inhibition of the sexual response • orgasmic (coital) difficulties • increasing dissatisfaction frank frustration with sexual intimacy.

35. Chronic pain, of whatever type, • destroys the vital energy • leaving the affected woman weak, fatigued, anergic, moody, fearfuldistressed, depressed, pessimistic up to a frank catastrophism

36. 1. in the couple: having a partner who complains of chronic genital pain is a challenge (a)sexual intimacy up to a complete avoidance of any intimate behavior; (b) it monopolizes the conversation and the life content around the vulvar pain and related symptoms; (c) it irritates, and causes anger, aggressiveness, verbal and physical abuses, when the physician tell the partner that “she has nothing, pain is all in her head,” or that “she is inventing pain”; or that she is “just trying to avoid intercourse (d) it has increasing costs: countable (for visits, exams, loss of working days) and uncountable (for the waste of life, the dark days, the depression, the loss of happiness within the relationship);

37. Central mechanism • Chronic pain is associated with changes in (CNS), which may maintain the perception ofpain in the absence of acute injury • the understandingof pain perception and has demonstrated that a complexseries of spinal, midbrain, and cortical structures are involvedin pain perception

40. Central mechanism. • the dorsal horn can have profound effect onpain sensation. Lamina IV and V of the dorsal horn containpeculiar neurons called (WDR). Repetitive stimulation by C-fibers causes some WDR cells inthe dorsal horn to augment their response. • Thus, for a giveninput stimulus, the output is enhanced; this process is referredto as “wind up.” Wind up is a part of a process termed “centralsensitization.”

41. Central mechanism • It was speculated that increased gray matter density couldbe caused by microglial proliferation, maybe due to excessexcitatory neural activity

42. Central sensitization • the central sensitization, • pivotal aspect of neuropathic pain. • involves an increase in the receptive fields of a nociceptor, • an increase in the magnitude and duration of response to a noxious stimulus. • a reduction in the threshold required to stimulate nociceptors

43. Peripheral change • after nerve damage. Free nerve endings injury induces structural and functional changes in both injured and uninjured parts of the nerve. • These changes increase ectopic and spontaneous firing after nerve damage, furthermore “cross-talk” from neighboring nerves can augment this effect. • Regeneration of axon terminals after nerve damage may enhance cross-talk, although the degree of sprouting does not correlate with the severity of pain behaviors.

44. generalized vulvodynia. • it is difficult to find a trigger inflammatory events in generalized vulvodynia. • Women with generalized vulvodynia experience symptomsanywhere within the distribution of the pudendalnerve. The pudendal nerve is an extrapelvic nerve; • it quicklyexits the pelvis, wrapps around ischial rectal fossa, enters thepudendalcanal, and provides innervation to the external genitalia, • the urethral sphincter • the anal sphincter, • the externalgenitalia.

45. A vestibular proliferation of C-afferent receptors (ten foldsincrease in the density of nerve endings) • a significant number ofactivated mast cells (assessed by measuring the mast cell degranulationlevels) has been reported in vestibulodynia patients.

46. Recent lines of evidence highlight a • potential genetic predispositionto chronic inflammation amongVestibulodyniaafflicted women. • These genetic polymorphism leads to a • reduced capacity to terminate and to an exaggerated inflammatoryresponse.

47. A reduced capacity to control Candidaalbicansaction due to a polymorphism in the gene codingfor mannose-binding lectin, an innate immune systemantimicrobialprotein, has been reported and this polymorphismhas also been associated with vestibulodynia کاهش ظرفیت کنترل کاندیدا آلبیکنس به علت پلی مورفیسم ژن کدگذاری برای لکتین اتصال دهنده مانوز، ذاتیپروتئین ضد میکروبی سیستم ایمنی گزارش شده است و این پلی مورفیسم نیز با ویستیبولودینیا همراه است

48. dyspareunia

50. The diagnosis of this pathological condition, namely GPPPD ,is prominently clinical based on: • 1. an extremely careful listening to the symptoms • “reading” of the sexual penetrationproblem(s) • 2. questioning with an investigative mind on predisposing, precipitating, and perpetuating factors, • while activating the mental file • « what is the pathophysiologic correlate of those factors? »