Alessandra Graziottin1, 2 and Filippo Murina3
(1)
Center of Gynecology and Medical Sexology, H. San Raffaele Resnati, Milan, Italy
(2)
Graziottin Foundation for the cure and care of pain in women, Italy
(3)
Department of Vulvar Disease V. Buzzi Hospital Obstetrics and Gynecological Clinic, University of Milan, Milan, Italy
Abstract
Vulvodynia (vulvar pain) and dyspareunia (painful intercourse) are closely related for anatomic, functional, pathophysiologic, emotional and relational reasons. Definitions of dyspareunia and vaginismus, also named ‘sexual pain disorders’ have varied in the past years.
Vulvodynia (vulvar pain) and dyspareunia (painful intercourse) are closely related for anatomic, functional, pathophysiologic, emotional and relational reasons. Definitions of dyspareunia and vaginismus, also named ‘sexual pain disorders’ have varied in the past years.
Box 1
Definition of Dyspareunia and Vaginismus
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Dyspareunia is defined as persistent or recurrent pain with attempted or complete vaginal entry and/or penile vaginal intercourse. |
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Vaginismus is defined as persistent or recurrent difficulties on the part of the woman in allowing vaginal entry of a penis, a finger, and/or any object, despite the woman’s expressed wish to do so. There is often (phobic) avoidance and anticipation/fear/experience of pain, along with variable involuntary pelvic-muscle contraction. Structural or other physical abnormalities must be ruled out/addressed. |
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The disorder may be: |
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lifelong vs acquired; |
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generalized vs contextual (i.e., limited to a specific partner and/or situation); |
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biological, psychogenic, or mixed. |
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The disorder may or may not cause personal distress. In the vast majority of cases, however, coital pain is a powerful trigger of personal and relational distress. |
Vulvodynia can trigger dyspareunia, and painful sexual intercourse may worsen or precipitate vulvar pain and help to maintain it (Fig. 3.1). The only exception is vulvodynia in children or virgin adolescents, or in women of any age who do not have penetrative sex.
Fig. 3.1
Coital pain is associated to an inflammated introital mucosa, this for many causes. We can observe a defensive hyperactive pelvic floor (myogenic hyperactivity) followed by the proliferation of pain nerve fibers with hyperalgesia and allodynia. When, on a normal vestibular mucosa, the initial symptom is coital pain, the first consequence is the defensive contraction of the levator ani (like in primary vaginismus and lifelong dyspareunia). This predisposes the introital vestibular mucosa to microabrasions resulting from the mechanical damage that can occur due to an attempt at sexual intercourse, with hyperactivation of mast cells and finally a proliferation of pain nerve fibers and vulvodynia
A lifelong hyperactive pelvic floor (‘myogenic hyperactivity’, which may or may not be associated with phobia of penetration) anatomically reduces the size of the entrance of the vagina. This predisposes the introital vestibular mucosa to microabrasions resulting from the mechanical damage that can occur due to an attempt at sexual intercourse. A contributing factor is inadequate genital arousal, due to the reflex inhibition that pain and/or fear of pain (whether lifelong or acquired) has on vaginal lubrication and vulvar congestion. Mechanical mucosal damage immediately activates the mast cell response: when attempts at intercourse are recurrent, and/or coital damage persistent, and/or if concomitant factors such as a Candida vaginitis further contribute to the inflammatory state, there can be three key consequences (also see Chapter 6):
1.
Hyperproduction of inflammatory molecules and neurotrophins such as nerve growth factor (NGF) by mast cells, which induces:
2.
proliferation of the pain nerve fibers responsible for introital hyperalgesia and allodynia, which in turn induces or worsens:
3.
hyperactivity of the pelvic floor.
This is a vicious circle that can also work in reverse: beginning with recurrent/chronic inflammation of the introital mucosa, caused by infection (e.g., from Candida, Herpes, Gardnerella), physical damage (laser therapy or diathermocoagulation), chemical irritation (from soaps, perfumes, douche gel or other substances), allergies, iatrogenic insults (episiotomy-rraphy, or any other perineal surgery such as the removal of a Bartholin’s cysts), life styles, such as the wearing of tight jeans, or neurogenic stimuli. These can induce the hyperactivation of the mast cell response, defensive contraction of the elevator ani (Fig. 3.2) and proliferation of pain nerve fibers via NGF.
Fig. 3.2
Symptoms and signs may be correlated by listening carefully to the woman and performing an accurate clinical examination
Over time, a close reciprocity between vulvodynia and dyspareunia comes into play. In more serious cases this induces the progression of vulvodynia from provoked (by any genital or sexual stimulus or gynecologic examination) to unprovoked, from localized to generalized (with progressive comorbidity with bladder symptoms), and from dyspareunia to acquired loss of desire, arousal difficulties (mental and genital), orgasmic difficulties, and progressive avoidance of intercourse (Fig. 3.3). This has important consequences for the woman and her partner as it impacts directly on their intimate physical and emotional relationship (see Chapter 5 for more details).
Fig. 3.3
Female Sexual Dysfunction (FSD) and dyspareunia. Coital pain (either due to vaginismus or other factors causing dyspareunia) directly inhibits vaginal lubrication, causing difficulties with genital arousal, vaginal dryness, orgasmic difficulties at intercourse, frustration, and dissatisfaction, and progressive avoidance of sexual intimacy in the majority of couples
Addressing Sexual Issues in the Clinical Setting
Despite the close relationship between vulvodynia and dyspareunia, physicians feel generally uncomfortable in investigating the sexual side of vulvodynia. This may be due to lack of training, fear of opening a Pandora’s box of complaints and concerns, lack of time, or worries about being perceived as acting inappropriately or invasively by asking about sex.
Consequently, only a small minority of physicians routinely ask about coital pain while investigating vulvar pain-related complaints. And even fewer recommend abstinence from intercourse until the goal of complete healing of the introital mucosa, adequate relaxation of the pelvic floor and complete disappearance of vulvar pain has been achieved. Continuation of sexual intercourse, a causative, predisposing, precipitating and maintining factor for dyspareunia and vulvodynia, contributes to the chronicity of pain and the shift between nociceptive and neuropathic pain. Other forms of sexual intimacy, such as foreplay, reciprocal masturbation or ‘outercourse’ may be enjoyed, however, at least in the less severe cases of vulvodynia.
Yet, there are key questions about sexual pain that must be asked if the significance and pathophysiology of vulvodynia are to be fully understood. When investigating the sexual side of vulvodynia, key recommendations include:
· raise the issue of sexuality when a general history is taken from the patient, beginning with a single, open-ended question, such as: “How’s your sexual life?” or, simply: “Do you feel pain during intercourse or do you have other sexual difficulties?” This demonstrates to the patient that the physician is comfortable with the issue and sees it as an important aspect of his or her health and well being, avoiding the ‘collusion of silence’ that can occur if the patient is too shy or reserved to discuss the topic, and the physician too concerned to raise the issue;
· take seriously any sexual concern, regardless of the patient’s age or medical status;
· be sensitive to gender and cultural factors, but do not make assumptions based on gender or cultural stereotypes when discussing sexual issues. Assume that every patient has his or her unique sexual history and needs;
· consider the role of the partner (if any) in the sexual relationship, and in any intervention keep an open mind about the dynamics of the couple’s relationship;
· devote special attention to confidentiality, informed consent, and consider the potential limits of confidentiality, such as in the reporting of sexual abuse, especially in younger patients;
· avoid emotionally loaded terms, such as “sexual abuse”. For example, ask the patient: “Have you ever had an unwanted sexual experience?” rather than, “Have you ever been sexually abused?”. This approach is much more likely to elicit such information. A patient may say, for example: “I was drunk the first time I had sex and have felt guilty about it ever since,” or, “I have had genital pain ever since”, thereby suggesting important psychosexual co-factors in the etiology and persistence of pain;
· last but not least, be aware of your own areas of comfort and discomfort when addressing sensitive sexual issues (Tables 3.1 and 3.2).
Table 3.1
The scenario for addressing sexual issues (modified from Plaut M et al., 2004)
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a) A proactive, empathic approach to your patient’s sexual life will convey an attitude of availability and acceptance. Sexual issues may be discussed in a number of contexts, including: - obtaining background information about sexual function; - addressing possible consequences of illness, injury, procedure, or medication and specifically the potential comorbidity between vulvodynia and dyspareunia; - the presentation by the patient of a sexual problem or question. |
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b) It takes courage to disclose a sexual dysfunction or a sexual trauma. Such disclosures should be taken seriously and addressed in a sensitive manner. |
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c) Patients may reflect a wide diversity of experiences, values, and preferences: - all people may have sexual interests or concerns, including the elderly, the disabled, and those with chronic illness, such as vulvodynia and other types of chronic pain; - be sensitive to gender and cultural differences, but do not assume that any one patient necessarily fits a gender or cultural stereotype; - whenever possible, involve both the symptomatic patient and the partner in evaluation and treatment. |
Table 3.2
Talking with patients about sexual issues (modified from Plaut M et al., 2004)
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- Be sensitive to the optimal time to ask the most emotionally charged questions; |
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- look for and respond to non-verbal cues that may signal discomfort, surprise, concern or pain; |
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- be sensitive to the impact of emotionally charged words (e.g. abortion, masturbation, rape); |
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- if you are not sure of the patient’s sexual orientation, use gender neutral language in referring to his or her partner; |
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- explain and justify your questions and procedures; |
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- teach and reassure as you examine, specifically explaining every step when making the physical examination and describing the pain map in vulvodynia patients; |
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- intervene to the extent that you are qualified and comfortable; refer to qualified medical or mental health specialists as necessary. |
Vaginismus and Dyspareunia: How Can they Contribute to Vulvodynia?
Although there is a longstanding tradition of distinguishing female sexual pain disorders into vaginismus and (superficial) dyspareunia, recent research has demonstrated persistent problems with the sensitivity and specificity of the differential diagnosis of these two phenomena.
Both complaints may comprise, to a smaller or larger extent:
a.
Problems with muscle tension: voluntary, involuntary, limited to vaginal sphincter, the bulbocavernous muscle, or extending to the pelvic floor, adductor muscles, back, jaws or entire body;
b.
Pain upon genital touching: superficially located at the vaginal entry, the vulvar vestibulum and/or the perineum; either event-related (to the duration of genital touching/pressure), or more chronic (lasting for minutes/hours/days after termination of touching); ranging from unique association with genital touching during sexual activity to more general association with all types of vulvar/vaginal/pelvic pressure (e.g., sitting, riding a horse or bicycle, wearing tight trousers);
c.
Fear of sexual pain: either specifically associated with genital touching/intercourse or more generalized fear of pain, or fear of sex;
d.
Propensity for behavioral approach or avoidance: despite painful experiences with genital touching/intercourse, a subgroup of women continues to be receptive to sexual interaction initiated by a partner or by themselves. This continuation of sexual interaction may have very different psychodynamic meanings. Whether a conscious or unconscious choice, it may help to maintain closer bonding but at the price of worsening mucosal inflammation. On the other hand it may be perceived as frank abuse if it is imposed by the partner. The majority of patients affected by dyspareunia and/or vulvodynia tend, however, to progressively avoid intercourse.
In summary, mild lifelong hyperactivity of the levator ani and other muscles of the pelvic floor, which may coincide with grade I or II vaginismus (according to Lamont, Table 3.3), may permit intercourse while causing coital pain, thus contributing to lifelong dyspareunia. Severe hyperactivity of the levator ani, with variable phobia of penetration, is defined as severe vaginismus: it prevents intercourse and is the most frequent cause of unconsummated relationship or marriage in women. However, as no consensus has been reached so far in unifying the two entities, they will be kept separate according to the latest classification.
Table 3.3
Degree of vaginismus, evaluated in a gynecological setting (grades). Modified from Lamont JA, 1978, with permission
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I Spasm of the elevator ani that disappears with reassurance of the patient |
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II Spasm of the elevator ani that persists during the gynecologic examination |
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III Spasm of the elevator ani and buttock tension at any attempt to perform gynecologic examination |
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IV Mild neurovegetative arousal, spasm of the elevator, dorsal arching, thighs adduction, defense and retraction |
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V Extreme defense and neurovegetative arousal, with refusal of the gynecologic examination |
Pathophysiology
Vaginal receptiveness is a prerequisite for intercourse, and requires anatomic and functional tissue integrity, both in resting and aroused states. The necessary biologic conditions to guarantee vaginal ‘habitability’ are shown in Table 3.4. Vaginal receptiveness may be further modulated by psychosexual, mental and interpersonal factors, all of which may result in poor arousal with vaginal dryness.
Table 3.4
Biological factors contributing to maintain vaginal ‘habitability’
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- Normal trophism, i.e., healthy introital mucosa and vulvar skin; |
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- adequate hormonal impregnation, with estrogen (vaginal) and testosterone (vulva); |
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- normal tonicity of the perivaginal muscles, levator ani first; |
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- vascular, connective and neurological integrity; |
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- normal local immune response; |
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- no signs or symptoms of inflammation, particularly at the introitus. |
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Fear of penetration, and a general muscular arousal secondary to anxiety, may cause a defensive contraction of the perivaginal muscles, leading to lifelong vaginismus. This disorder may also be the clinical correlate of a primary neurodystonia of the pelvic floor, as recently demonstrated with needle electromyography. It may be so severe as to prevent penetration completely. Vaginismus is the leading cause of unconsummated marriages or relationships in women. Comorbidity between lifelong vaginismus and dyspareunia (see Fig. 3.1), and other female sexual dysfunction, is frequently reported. The defensive pelvic floor contraction may also be secondary to genital pain, of whatever cause. Dyspareunia is the common symptom of a variety of coital pain-causing disorders (Table 3.5). Vulvar vestibulitis (VV), a subset of vulvodynia, is its leading cause in women of fertile age. The diagnostic triad is: 1) severe pain upon vestibular touch or attempted vaginal entry; 2) exquisite tenderness to cotton-swab palpation of the introital area (mostly at 5 and 7, when looking at the introitus as a clock face); 3) dyspareunia (see Chapter 6). Painful outcomes of episiotomy-rraphy and/or vulvar/perineal tears are the second (and neglected) cause of dyspareunia during the puerperium (see Capter 4). |
Table 3.5
Etiology of dyspareunia: different causes may overlap, with complex and dynamic pathophysiologic interplay (adapted from Graziottin A, 2005)
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A) Biological |
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1) Superficial/introital and/or mid-vaginal dyspareunia |
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- infectious: vulvitis, vulvar vestibulitis, vaginitis, cystitis; |
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- inflammatory: with mast cell up-regulation; |
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- hormonal: vulvo-vaginal atrophy; |
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- anatomical: fibrous hymen, vaginal agenesis, Rokitansky syndrome; |
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- muscular: primary or secondary hyperactivity of levator ani muscle; |
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- iatrogenic: poor outcome of genital or perineal surgery; pelvic radiotherapy; |
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- neurologic, inclusive of neuropathic pain; |
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- connective and immunitary: Sjogren’s syndrome; |
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- vascular; |
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- female genital mutilation, with introital/vaginal narrowing. |
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2) Deep dyspareunia |
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- endometriosis; |
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- Pelvic Inflammatory Disease (PID); |
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- chronic pelvic pain and referred pain; |
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- pelvic varicocele; |
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- outcome of pelvic radical surgery or endovaginal radiotherapy; |
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- Abdominal Cutaneous Nerve Entrapment Syndrome (ACNES). |
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B) Psychosexual |
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- comorbidity with desire and/or arousal disorders, or vaginismus; |
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- past sexual harassment and/or abuse; |
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- affective disorders: depression and anxiety; |
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- catastrophism as leading psychological coping modality. |
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C) Context or couple related |
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- lack of emotional intimacy; |
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- inadequate foreplay; |
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- couple’s conflicts; verbally, physically or sexually abusive partner; |
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- poor anatomic compatibility (penis size and/or infantile female genitalia); |
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- sexual dissatisfaction and consequent inadequate arousal. |
Clinical Approach: Taking a Clinical History
In sexual pain disorders, an accurate clinical history and careful physical examination are essential for ascertaining a diagnosis and a prognosis. The location and characteristics of pain have been demonstrated to be the most significant predictors of its etiology. No instrumental exam has so far been demonstrated to be more informative than a carefully performed clinical examination.
Focusing on the presenting symptom - dyspareunia - and with the abovementioned attention to the sensitivity of the issue, the key questions required to obtain the most relevant information can be summarized as follows:
· Did you experience coital pain from the very beginning of your sexual life onwards (lifelong) or did you experience it after a period of normal (painless) sexual intercourse (acquired disorder)?
· (If lifelong) Were you afraid of feeling pain before your first intercourse?
Key point: When lifelong, dyspareunia is usually caused by mild/moderate vaginismus (which causes painful penetration) and/or coexisting, life-long low libido and arousal disorders.
· (If acquired) Do you remember the situation or what happened when it started?
Key point: The answer can give information about the “natural history” of the current sexual complaint, and the “personal reading” the woman has of her problem, of significant co-factors and meaning.
· Where does it hurt? At the beginning of the vagina, in the mid vagina or deep in the vagina?
Key point: The location of pain and its onset within an episode of intercourse is the strongest predictor of presence and type of organicity.
· introital dyspareunia may be more frequently caused by poor arousal, mild vaginismus, vulvar vestibulitis, vulvar dystrophia, painful outcome of vulvar physical therapies, perineal surgery (episiorraphy, colporraphy, posterior perineorraphy), female genital mutilation with introital/vaginal narrowing, pudendal nerve entrapment syndrome and/or pudendal neuralgia, Sjogren’s syndrome;
· mid-vaginal pain, acutely evoked during physical examination by a gentle pressure on the sacro-spinous insertion of the levator ani muscle, is more frequently due to levator ani myalgia, the most frequently overlooked biological cause of dyspareunia;
· deep vaginal pain may be caused more frequently by endometriosis, chronic pelvic pain or pelvic inflammatory disease (PID) or by outcomes of pelvic radiotherapy or vaginal radical surgery. Varicocele, adhesions, referred abdominal pain, and abdominal cutaneous nerve entrapment syndrome (ACNES) are less frequent and still controversial causes of deep dyspareunia, which should nevertheless be considered in the differential diagnosis.
· When do you feel pain? Before, during or after intercourse?
Key point: the timing of pain with respect to intercourse is critical in understanding the cascade of pathophysiologic events, the potential relationship between vaginismus and dyspareunia and leading comorbidities.
· pain before intercourse suggests a phobic attitude towards penetration, usually associated with vaginismus, and/or the presence of chronic vulvar vestibulitis, clitoralgia and/or vulvodynia, which may also facilitate pain in the arousal state during foreplay and before penetration;
· pain during intercourse is more frequently reported. This information, combined with the previous question, “Where does it hurt?”, is the most predictive of the organicity of pain;
· pain after intercourse indicates that mucosal damage was provoked during intercourse, possibly because of poor lubrication, leading to vestibulitis, pain and defensive contraction of the pelvic floor.
· Do you feel other accompanying symptoms, vaginal dryness, pain or abnormal sensation in the genitals and pelvic areas? Or do you suffer from cystitis 24–72 hours after intercourse?
Key point: attention to accompanying symptoms is key for the early diagnosis of comorbidities and appropriate understanding of the pathophysiology of the current complaint(s).
· vaginal dryness, either secondary to loss of estrogen and/or to poor genital arousal may coincide with/contribute to dyspareunia;
· clitoralgia and/or vulvodynia, spontaneous and/or worsening during sexual arousal may be associated with dyspareunia, hypertonic pelvic floor muscles, and or neurogenic pain, inclusive of pudendal nerve entrapment syndrome;
· post-coital cystitis should suggest a hypoestrogenic condition and/or the presence of hypertonic pelvic floor muscles: it should specifically be investigated in young women complaining of ‘burning bladder’ symptoms (and syndrome) in comorbidity with dyspareunia; and in post-menopausal women who may benefit from topical estrogen treatment and rehabilitation of the pelvic floor, aimed at relaxing the myalgic perivaginal muscles;
· vulvar pruritus, vulvar dryness and/or feeling of a burning vulva should be investigated, as they may suggest the presence of vulvar lichen sclerosus, which may worsen introital dyspareunia. Neurogenic pain may cause not only dyspareunia but also clitoralgia. Eye and mouth dryness, when accompanying dyspareunia and vaginal dryness, should suggest Sjogren’s syndrome.
· How intense is the pain you feel?
Key point: Focusing on the intensity and characteristics of pain is relatively new approach in addressing dyspareunia. A shift from nociceptic to neuropathic pain is typical of chronic dyspareunia, and treatment may require a systemic and local analgesic approach.
Practical Tips
Suggest patient keeps a diary of pain, mirroring the menstrual cycle phases if the woman is in her fertile age (i.e., starting every page with the first day of her cycle, with the date on the x axis, and the 24 hours of the day in the y axis. Pain intensity could be reported with three colours: zero pain = white; 1 to 3 = yellow; 4 to 7 = red; 8 to 10 (worst pain ever) = black).
This will: 1) improve the recording and understanding of pain flares before, during and/or after the menstrual cycle, and the circadian rhythm of pain, to improve the diagnosis, etiology and contributors of pain; 2) suggest a better way to tailor the analgesic treatment; 3) make more accurate the recording of the impact of treatment on pain perception. Typically, nociceptive pain persists and worsens at night, while neuropathic pain is significantly reduced or absent during sleep.
Conclusions
Pain is rarely purely psychogenic, and dyspareunia is no exception. Like all pain syndromes, it usually has one or more biologic etiologic origins. Hyperactive pelvic floor disorders are a constant feature and comorbidity with urologic and/or proctologic disorders is a frequent and yet neglected area to be explored for comprehensive treatment.
Psychosexual and relationship factors, generally lifelong or acquired low sexual desire because of persistent pain, and lifelong or acquired arousal disorders due to the inhibitory effect of pain, should be addressed in parallel, in order to provide comprehensive, integrated and effective treatment.
Vaginismus, which may contribute to lifelong dyspareunia, when mild/moderate, and may prevent intercourse, when severe, needs to be better understood in its complex neurobiologic, muscular and psychosexual etiology, and addressed via a multimodal approach.
In patients with vaginismus, the diagnosis and prognosis may be madebased on three variables:
· intensity of phobic attitude (mild, moderate, severe) toward penetration;
· intensity of pelvic floor hypertonicity (in four degrees, according to Lamont);
· co-existing personal and/or relational psychosexual problems.
Relationship issues should be diagnosed and appropriate referral considered when the male partner presents with a concomitant male sexual disorder.