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Sexual dysfunction 

Sexual dysfunction
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Sexual dysfunction
Author(s):

Ian Eardley

DOI:
10.1093/med/9780199204854.003.130805
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Essentials

Male sexual dysfunction

Erectile dysfunction—the inability to attain or maintain an erection satisfactory for sexual intercourse. It affects about 50% of men over the age of 40 years and can be caused by neurological, vascular, endocrine, and psychiatric diseases, and by drugs, with psychogenic and organic risk factors coexisting in most men. Specific remedies can cure erectile dysfunction in a few patients: the mainstay of treatment in most will be oral therapy using a phosphodiesterase type 5 inhibitor.

Penile deformity—usually due to Peyronie’s disease: there is no licensed medical therapy and treatment is by surgical correction of any debilitating deformity.

Prolonged erection (priapism)—this is a medical emergency, requiring urgent therapy to prevent loss of erectile function. Most cases are caused by reduced venous drainage of the corpus cavernosum, most commonly due to intracavernosal injections, sickle cell disease, other hyperviscosity syndromes, or the use of some psychotropic drugs. Treatment initially involves aspiration via a wide bore cannula of enough blood to produce detumescence.

Premature ejaculation—a common but poorly understood condition that has no licensed medical therapies and is best treated with psychosexual therapy.

Female sexual dysfunction

Hypoactive sexual desire—may affect up to one-third of women under the age of 50 years: its aetiology is commonly multifactorial, including complex interaction with relationship issues, and the motivation for and success of treatment is low.

Sexual arousal disorders—affect up to one-quarter of women and may be caused by psychological or physical factors: treatment is directed towards the predominant aetiological issues.

Anorgasmia—reported by up to 37% of women in association with many psychological and cultural influences: therapy is primarily psychosexual, particularly when the problem is lifelong.

Dyspareunia—reported by up to 15% of sexually active women and can be caused by organic, psychological, or couple-related factors. Vaginismus affects less than 1%, with vulvar vestibulitis the most common cause: treatment is often unsatisfactory.

Male sexual dysfunction

Male sexual function is a complex neurovascular event that can be affected by a number of disease processes resulting in problems of penile erection, ejaculatory difficulties, and disorders of desire. Of these, the most common dysfunctions encountered in clinical practice are erectile dysfunction, penile deformity, prolonged erections, and rapid (or premature) ejaculation.

Erectile dysfunction

Erectile dysfunction is defined as the inability to attain or maintain an erection satisfactory for sexual intercourse. The first modern (and perhaps most important) epidemiological study was the Massachusetts Male Aging Study, which reported the age-related prevalence in North American men. It is a common symptom that affects around 50% of men over the age of 40 years. The prevalence increases with age, and there are associations with a range of conditions including diabetes, hypertension, dyslipidaemia, and depression.

The physiology of penile erection is complex and involves the coordinated interaction of the neurological, vascular, and endocrine systems. Hence, there are many diseases of these systems that can lead to the development of erectile dysfunction, some of which are listed in Table 13.8.5.1. It is now recognized that both psychogenic and organic risk factors coexist in most men with erectile dysfunction, albeit to varying degrees. Secondary performance related anxiety often complicates the pathophysiology of men who have a primary organic aetiology. The most common cause of erectile dysfunction is that which arises secondary to vascular disease, with erectile dysfunction being a common coexisting symptom in men with hypertension, diabetes, hyperlipidaemia, and cardiovascular disease. Indeed, there is emerging evidence that erectile dysfunction may be one of the very earliest features of systemic vascular disease.

Table 13.8.5.1 Common causes of erectile dysfunction

System

Disease

Neurological disease

  • Multiple sclerosis

  • Spinal cord injury

  • Multiple system atrophy

  • Lumbar disc prolapse

  • Cauda equina syndrome

  • Peripheral autonomic neuropathy (e.g. diabetes)

Vascular disease

  • Atherosclerosis

  • Hypertension

  • Hyperlipidaemia

  • Diabetes

Endocrine disease

  • Diabetes mellitus

  • Hypogonadism

  • Hyperprolactinaemia

  • Hyperthyroidism

Psychiatric disease

  • Depression

  • Anxiety states

Iatrogenic

  • Pelvic surgery (with nerve damage)

  • Pelvic radiotherapy

  • Drugs (see Table 13.8.5.2)

Multifactorial aetiologies

Renal failure

Since erectile dysfunction is a self-declared symptom, the fundamental basis of diagnosis is the clinical history. Mild cases are characterized by a history of difficulty in maintaining an erection, while in more severe cases there may be difficulty in initiating an erection or even loss of erections altogether. Assessment should seek to identify treatable causes (see Tables 13.8.5.1 and 13.8.5.2) and remediable risk factors. A predominantly psychogenic aetiology is suggested by the continued presence of nocturnal or early morning erections. Current guidelines suggest a focused physical examination of the genitalia, assessment of secondary sexual characteristics, and assessment of blood pressure. More extensive genitourinary and vascular examination is only performed when clinically indicated. Baseline investigations should include a fasting blood sugar, a lipid screen, and measurement of serum testosterone. The role of routine measurement of serum prolactin is controversial. Further assessment is usually unnecessary, although in selected cases vascular investigations (including colour Doppler assessment of penile vasculature) and more complex endocrine investigations might be indicated.

Table 13.8.5.2 Drugs that can cause sexual dysfunction in men

Drug type

Drug or class of drug

Effect

Antihypertensive drugs

  • Diuretics

  • Beta-Blockers

  • Centrally acting anti-hypertensive agents e.g. clonidine, methyl DOPA

  • ED

  • ED

  • ED

Centrally acting agents

  • Phenothiazines

  • Butyrophenones

  • Serotonin reuptake inhibitors

  • Tricyclic antidepressants Phenytoin

  • ED, Reduced libido, Ejaculatory dysfunction

  • ED

  • ED, Ejaculatory dysfunction

  • ED, Reduced libido

  • ED, Reduced libido

Endocrine drugs

  • LHRH analogues Antiandrogens

  • Oestrogens

  • ED, Reduced libido

  • ED, Reduced libido

  • ED, Reduced libido

Recreational drugs

  • Alcohol

  • Marijuana

  • Cocaine

  • Opiates

  • Amphetamines

  • Anabolic steroids

  • ED, Reduced libido, Ejaculatory dysfunction

  • ED

  • ED

  • ED, Reduced libido

  • Reduced libido, Ejaculatory dysfunction

  • ED, Reduced libido

Other drugs

  • Cimetidine

  • Metoclopramide

  • Digoxin

  • ED, Reduced libido

  • ED, Reduced libido

  • ED

Specific remedies can cure erectile dysfunction in a few patients. For instance, in men with a predominantly psychogenic aetiology, psychosexual counselling is often valuable. In men with an endocrine cause (such as hypogonadism or hyperprolactinaemia), appropriate therapy is also helpful. Finally, in men who have developed erectile dysfunction following pelvic or perineal trauma, reconstructive vascular surgery may be effective. In most men, however, treatment aims to treat the symptom, rather than curing the underlying problem. Given the prevalence of secondary psychogenic problems, patient education and counselling is always valuable, but in most men who present with erectile dysfunction the mainstay of therapy will be oral therapy using a phosphodiesterase-5 inhibitor (PDE5i). Sildenafil was the first such licensed preparation, and two other drugs—tadalafil and vardenafil—have been marketed in recent years. There appears to be little difference in efficacy and tolerability between these drugs, with the major differences relating to pharmacokinetics. The drugs are used on demand, with ingestion 1 to 2 h prior to sexual activity. They are ineffective in the absence of sexual stimulation and a heavy meal may delay absorption. Around 70 to 80% of men will respond to such therapy, although the response rate is lower in some patient groups, such as diabetics and men who have undergone radical pelvic surgery. Side effects include headache, flushing, indigestion, and nasal congestion, although these are usually mild and well tolerated. Prolonged erections are seen extremely rarely with these drugs. Extensive research has not identified any significant cardiac risk with this class of drugs, although they are contraindicated in men using nitrate medication, and sexual activity is inadvisable in men with unstable cardiac disease. A detailed summary of the management of erectile dysfunction in men with cardiac disease can be found in the Princeton Consensus Statements.

In men with identifiable risk factors for erectile dysfunction, or an identifiable aetiology, there is only limited evidence that treatment of the risk factors provides benefit. One randomized trial suggested that weight reduction in men who had a raised body mass index might be beneficial over a 2 year period, although the improvements seen were limited.

In men who fail to respond to oral PDE5i therapy, a number of approaches can be tried, although there is little evidence that use of a different PDE5i is beneficial. Regular (daily) dosing appears to help some patients, the rationale reflecting experimental evidence that a PDE5i might improve endothelial function when taken regularly. Alternatively, optimization of coexistent medical conditions is occasionally helpful in this respect. In men who fail to respond to these manoeuvres, alternative therapies such as vacuum erection devices or intracavernosal self-injection of alprostadil are often effective. In a few patients even these treatments are ineffective or poorly tolerated, and under these circumstances insertion of a penile prosthesis may be indicated.

Penile deformity and Peyronie’s disease

Although young men or adolescents occasionally present with a lifelong penile deformity (congenital curvature of the penis), the most common cause of penile deformity is Peyronie’s disease, which is a localized connective tissue disease of the penis leading to fibrotic plaque formation in the tunica albuginea of the corpus cavernosum. It was first described by Fallopius in 1561, although the condition is named after François Gigot de la Peyronie, surgeon to King Louis XV of France, who described it in 1743.

In pathological studies there is subclinical disease in over 20% of men, but the clinical prevalence is about 1%. In some cases the condition can be familial, and there are associations with Dupuytren’s contracture, plantar fasciitis, and tympanosclerosis. The peak incidence occurs in the 6th decade, but cases have been reported throughout adult life. The pathophysiology is poorly understood, but the most commonly held view suggests that there is damage of the tunica albuginea associated with microvascular trauma. This leads to extravasation and perivascular inflammation with a round cell infiltrate, which in turn leads to fibrin deposition and subsequently fibrosis.

Patients present with a palpable plaque within the penis, most commonly felt on the dorsum, and there is a curvature of the penis, most commonly in the dorsal direction. The disease typically progresses over 9 to 18 months, during which time it is said to be active. During this time the erection may be painful, the size of the plaque typically increases, and the deformity worsens until the disease stabilizes. When this happens, up to 20% of patients will get significant resolution of their deformity, and in only 30% of cases is the deformity significant enough to justify surgery.

Numerous medical treatments have been tried in men with Peyronie’s disease. The oral agents that are most commonly used in clinical practice are Vitamin E, tamoxifen, colchicine, and potassium aminobenzoate, but controlled studies have failed to demonstrate a consistent benefit for any of them. The most commonly used intralesional (injectable) agents are steroids, verapamil and collagenase, and although some recent data from controlled studies suggests that the latter may be beneficial, further controlled studies are awaited.

Surgical treatment is reserved for those patients whose penile deformity prevents sexual activity, or those in whom sexual activity is painful either for the patient or his partner. The disease must be stable prior to surgical intervention, since disease progression after corrective surgery should be avoided. The most common surgical approach is a Nesbit’s procedure, which involves surgical excision of an ellipse of a tunica albuginea on the opposite side of the penis to the plaque. The edges of the ellipse are apposed. Occasionally, a grafting procedure can be performed whereby the plaque is incised and grafted, typically with a patch of saphenous vein. A penile prosthesis is indicated in severe cases associated with coexistent erectile dysfunction.

Priapism

A priapism is a penile erection which is unduly prolonged and which persists in the absence of a sexual stimulus. The classification of priapism divides cases into those where the aetiology is arterial (high flow priapism) and those cases where the aetiology reflects reduced venous drainage of the corpus cavernosum (low flow priapism).

Low flow priapism is by far the more common form and reflects stasis of blood within the penis, with sludging within the cavernosal sinusoids and subsequent thrombosis. Ischaemia, hypoxia, and acidosis develop as a consequence, and this in turn prevents contraction of the penile smooth muscle, which then exacerbates the condition. Low flow priapism is a medical emergency and requires urgent treatment to avoid irreversible damage to the vascular endothelium and smooth muscle of the penis and its erectile capacity. Although comprehensive evidence is lacking, there are data to suggest that if treatment is successful within 24 h, then 56% of men will recover erectile function, while if treatment is delayed beyond that only 11% will recover potency. Low flow priapism can arise under a number of circumstances (see Table 13.8.5.3), the most common causes including intracavernosal injections, sickle-cell disease, other hyperviscosity syndromes, and the use of some psychotropic drugs.

Table 13.8.5.3 Causes of low flow priapism

Type

Example

Hypercoagulability disorders

  • Sickle-cell disease

  • Myeloma

  • Leukemia

  • Thalassaemia

  • Total parenteral nutrition

Drugs

  • Intracavernosal agents (e.g. alprostadil)

  • Psychotropic agents (e.g. phenothiazines, butyrophenones, trazodone)

  • Anticoagulants (e.g. warfarin, heparin)

  • Antihypertensives (e.g. α‎-blockers, calcium channel blockers)

Miscellaneous

  • Lumbar disc disease

  • Solid tumours affecting the base of the penis

  • Genito-urinary sepsis

  • Amyloidosis

Men with low flow priapism typically present with a painful erection, in contrast to high flow priapism which is painless, but a careful assessment should seek to differentiate low flow from high flow disorders (Table 13.8.5.4) and to identify the underlying cause. Aspiration of penile blood in low flow priapism reveals thick dark venous blood, which on blood gas analysis shows hypoxia, hypercapnia, and acidosis. Doppler scanning confirms lack of blood flow within the penis.

Table 13.8.5.4 Features that help to differentiate low flow from high flow priapism

Findings

Low flow priapism

High flow priapism

History of perineal trauma

Rare

Common

History of coexistent blood disorder

Sometimes

Rare

History of recent intracavernosal injection

Sometimes

Rare

Corpora cavernosa rigid

Usually

Rare

Penile pain

Usually

Rare

Cavernosal blood gases

Hypoxia, hypercapnia, acidosis

Similar to arterial blood

Colour Doppler penis

Sluggish or absent flow

Normal flow with evidence of arterial turbulence

Treatment for priapism initially involves aspiration via a wide bore cannula of enough blood to produce detumescence, followed if necessary by irrigation with warm heparinized normal saline (see Figs. 13.8.5.1 and 13.8.5.2). If the erection reappears, then intracavernosal injection of a smooth muscle α‎-agonist such as phenylephrine is appropriate, with concurrent monitoring of the systemic blood pressure. A surgical shunting procedure is appropriate if this fails. However, if treatment is delayed too long (see above), then even shunting procedures fail and the only hope for long-term potency is a penile prosthesis.

Fig. 13.8.5.1 Treatment of low flow priapism.

Fig. 13.8.5.1
Treatment of low flow priapism.

Fig. 13.8.5.2 Sites for safe aspiration of blood from the penis in low flow priapism are between 1 and 3 o’clock and between 9 and 11 o’clock.

Fig. 13.8.5.2
Sites for safe aspiration of blood from the penis in low flow priapism are between 1 and 3 o’clock and between 9 and 11 o’clock.

When there is a specific coexistent condition, such as sickle-cell disease, specific treatment may be appropriate alongside treatment of the priapism. However, the traditional regimen of oxygen, intravenous hydration, and analgesia is often unsuccessful, and only in selected cases is exchange transfusion indicated.

High flow or nonischaemic priapism develops following perineal trauma, when the penile artery is lacerated, resulting in a fistula between the artery and the sinusoidal spaces of the penis. The priapism may appear at the time of injury, but more commonly develops some time later following relief of spasm of the artery. Because the blood flowing through the penis is arterial (i.e. there is no ischaemia), there can be some circumspection in relation to treatment. The diagnosis is usually made by Doppler scanning and subsequent selective pudendal arteriography, which typically shows an arterial blush in the penile artery. The treatment of choice is embolization of the fistula with autologous blood clot.

Rapid (premature) ejaculation

There is no universally accepted definition of premature ejaculation, which has plagued attempts to assess the prevalence of the condition, with some data suggesting that it is probably the most common of the male sexual dysfunctions, affecting between 21% and 32% of adult men. One approach to achieving an objective diagnosis has been to measure the intravaginal ejaculatory latency time, i.e. the time between vaginal penetration and ejaculation, but once again there is no clear consensus as to which time should be the cut-off between normal and abnormal, with 1 min and 2 min both being reported in the literature. Epidemiological data suggest that when the definition given to the condition by the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders (4th edition) is used, then men with a diagnosis of premature ejaculation have a much shorter intravaginal ejaculatory latency time than normal men (1.8 min vs 7.3 min).

Premature ejaculation is traditionally categorized into primary (lifelong) and secondary (acquired) types. The aetiology is poorly understood, with many potential pathophysiological mechanisms being proposed and none proven. Many men with premature ejaculation do not seek treatment, although there is evidence that there can be deleterious effects upon self-esteem, interpersonal relationships, and quality of life. When patients do seek medical attention, it is important to look for coexistent sexual dysfunctions (erectile dysfunction is commonly present) and to assess the degree to which relationship issues are important.

Therapy usually involves sex therapy and psychotherapy in the first instance. Although commonly successful in the short term, such approaches may not lead to a long-term cure. Currently there are no licensed pharmacological treatments for premature ejaculation, although there is some evidence that both selective serotonin re-uptake inhibitors and PDE5is may have a role. A number of pharmacological agents are currently undergoing development, including topical local anaesthetic sprays and short acting selective serotonin re-uptake inhibitors.

Female sexual dysfunction

The sexual problems of women have, until recently, received much less attention from the medical and scientific community than male sexual problems. This is reflected in a less well developed understanding of physiological and pathophysiological processes, in a less well defined classification of dysfunctions, and in a smaller range of therapeutic interventions. One classification of female sexual dysfunction is shown in Table 13.8.5.5. Epidemiological studies, although relatively immature, suggest that female sexual disorders are common and that they relate in part to age and to hormonal status. Comorbidities are common and should be identified, and the different sexual dysfunctions commonly coexist.

Table 13.8.5.5 A classification of female sexual dysfunction

Category

Subcategory

Disorders of desire

  • Interest desire disorders

  • Sexual aversion disorders

Disorders of arousal

  • Subjective arousal disorders

  • Genital arousal disorders

  • Combined subjective and genital arousal disorders Persistent arousal disorder

Orgasmic disorders

Pain disorders

Dyspareunia Vaginismus

Sexual desire disorders

Hypoactive sexual desire disorder can be defined as absent or diminished feelings of sexual interest or desire, absent thoughts or fantasies, and a lack of responsive desire. This lack of interest will be greater than that which is normally seen with ageing and with the length of a relationship.

Epidemiological studies suggest that it affects up to 32% of women under the age of 50 years. It becomes more common with increasing age and with the onset of the menopause, whether natural or surgically induced. Around half of the women who have this condition are distressed by it, with the degree of distress diminishing with increasing age. Women with a surgically induced menopause are more likely to be distressed than those who have undergone a more natural menopause.

The physiology and pathophysiology of desire is poorly understood, but probably resides biologically in the limbic system of the brain, where hormonal influences, including oestrogens and androgens, are important. Other hormonal abnormalities including hyperprolactinaemia and thyroid dysfunction can also result in sexual desire disorders. The dominant neurotransmitters include dopamine, which is important in the seeking–appetite–lust system, and oxytocin, although as yet no pharmacological agents have any proven value. Other biological issues that are sometimes important include alcohol and recreational drug abuse. Psychological factors are also important in this condition, and their interaction with the biological issues makes this condition notoriously difficult to treat.

Clinical assessment includes a careful clinical history, which seeks to identify any psychological or physical issues. A full endocrine evaluation may be appropriate, which will include the measurement of serum testosterone, dehydroepiandrosterone sulphate, prolactin, 17β‎-oestradiol, and sex hormone-binding globulin.

Treatment is difficult and often unsuccessful, partly because the aetiology is commonly multifactorial, partly because of the complex interaction with relationship issues, but also because the motivation to be treated is often relatively low. Where physical causes can be identified, they should be treated, and indeed outcomes are best in the group of patients who have definite endocrine abnormalities and who are highly motivated. In other groups the results of therapy are often disappointing.

Sexual aversion disorders

Defined as severe anxiety or disgust at the thought of sexual activity, sexual aversion disorder may arise as a result of incest, rape, molestation, and psychological abuse. It may coexist with other anxiety disorders. Psychosexual therapy is the mainstay of treatment.

Sexual arousal disorders

Female sexual arousal includes the physiological responses of increased blood flow to the clitoris, the labia, and the vagina, leading to vasocongestion and engorgement. Vaginal lubrication appears to be a purely hydrostatic event, with transudation from the vaginal capillaries into the extracellular space. The physiology of these responses is poorly understood, but involves parasympathetic activation, with release of a number of neurotransmitters of which vasoactive intestinal peptide and nitric oxide are almost certainly the most important. There is concurrent relaxation of the vaginal smooth muscle with lengthening and dilation of the vagina. Systemically, there is an increase in the heart rate, flushing, and erection of the nipples.

There are three categories of arousal disorder. First, there is the so-called subjective arousal disorder, associated with a reduction in the feelings of sexual arousal (including sexual excitement and sexual pleasure), but with normal vaginal lubrication still occurring. Secondly, there may be genital sexual arousal disorder, when there is a definite and reduced degree of genital arousal in response to a sexual stimulus. Thirdly, the two may be found in combination.

Sexual arousal disorders are relatively common in the female population, affecting up to 24% of women. They are more common in older women, especially after the menopause, and the aetiology may be multifactorial. Psychological factors include reduced desire, sexual inhibition, anxiety, lack of intimacy, and male erection problems. Physical factors that may be important include endocrine abnormalities (e.g. reduced oestrogens, hyperprolactinaemia), vascular disease (e.g. diabetes), neuropathy (e.g. diabetes, multiple sclerosis), iatrogenic problems (e.g. post hysterectomy, post pelvic radiotherapy), and pain disorders (e.g. genital pain such as vaginismus, bladder pain due to recurrent urinary tract infection or interstitial cystitis).

Assessment should involve a careful history and examination, seeking to identify the range of risk factors that are present in an individual. Investigations might include an endocrine screen and, when indicated, Doppler assessment or plethysmography can evaluate vaginal and clitoral blood flow.

Treatment should be directed towards the predominant aetiological issues. Psychosexual methods are important for cases where subjective problems predominate. Physical treatments that may be of value include local lubricants, topical oestrogens (when vaginal atrophy and oestrogen deficiency are present), and local physical devices analogous to the vacuum erection devices used in male erection difficulties. Systemic hormone replacement therapy may be appropriate in some, but there are no licensed nonhormonal therapies for this condition. Given the physiological finding that nitric oxide is important in the control of vaginal blood flow, it was thought that the phosphodiesterase inhibitors such as sildenafil might have a role, but the results of clinical trials were relatively disappointing, and clinical development of these drugs for women has been halted.

Persistent sexual arousal disorder

This is a poorly documented but uncommon condition characterized by persistent genital arousal in the absence of a sexual stimulus. The pathophysiology is unknown, and as such there is no recognized therapy.

Orgasmic disorders in women

Anorgasmia is reported in up to 37% of women, and in some women there may be marked delay or decrease in the intensity of the orgasm. The female orgasm is characterized by a transient sensation of intense pleasure, associated with rhythmic contractions of the pelvic floor musculature, often associated with uterine and anal muscular contractions. Although the nature of the orgasm changes with age (becoming shorter and less intense), there is no evidence that the prevalence of orgasmic disorders becomes more common with increasing age.

The physiology of the female orgasm is poorly understood, but in most cases involves clitoral stimulation, in association with an intact sacral reflex arc. Although it would seem logical that intact ascending neural pathways are necessary for a woman to experience an orgasm, patients with complete spinal cord transection can, on occasions, have the experience, hence it has been suggested that ascending fibres within the vagus nerve may be important.

There are multiple psychological and cultural influences on the ability of a woman to experience an orgasm. For instance, there is an inverse relationship between the degree to which a woman holds serious religious views and her ability to experience an orgasm. From a physical perspective, arousal disorders can result in delayed or absent orgasm. As such, therapy is primarily psychosexual, particularly when the problem is lifelong. When the problem is more recent in onset and associated with a physically induced sexual arousal disorder, then therapy should be directed at the arousal disorder. No pharmacological agents have shown any value in the treatment of this condition.

Sexual pain disorders in women

Dyspareunia is pain associated with attempted or complete vaginal entry; vaginismus indicates difficulties in the woman allowing entry of a penis (or any other object) into the vagina, despite her desire for this to happen. It is traditional to separate these two conditions, although in reality they may overlap, both in causality and in clinical presentation. Dyspareunia is reported by up to 15% of sexually active women, and it becomes much more common in the postmenopausal population. Vaginismus is far less common, affecting less than 1% of sexually active women.

Dyspareunia can be caused by a number of different conditions (see Table 13.8.5.6), and while these conditions can also cause vaginismus, there are cases where no clear organic aetiology appears to exist. Clinically, it is important to identify such causes when they do exist, and to identify and treat any sexual comorbidities.

Table 13.8.5.6 Causes of dyspareunia

Organic

Superficial and introital

  • Infections (vulvitis, vulvar vestibulitis, cystitis, vaginitis)

  • Hormonal (vaginal atrophy)

  • Anatomic (fibrous hymen, vaginal agenesis)

  • Muscular (hyperactivity of levator ani)

  • Iatrogenic (post surgical, post radiation)

  • Neuropathic

Deep

  • Endometriosis

  • Pelvic inflammatory disease

  • Chronic pelvic pain syndrome

  • Iatrogenic (postsurgical, postradiation)

Psychological

  • Comorbidity with other disorders of female sexual function Previous sexual abuse or rape

  • Depression and anxiety

Couple related

  • Inadequate foreplay

  • Couple conflicts

  • Sexual dissatisfaction

  • Anatomical compatibility issues

Further reading

Male sexual dysfunction

Feldman HA, et al. (1994). Impotence and its medical and psychosocial correlates: results of the Massachusetts Male Aging Study. J Urol, 151, 54–61.Find this resource:

Fonseca V, Jawa A (2005). Endothelial and erectile dysfunction, diabetes mellitus, and the metabolic syndrome: common pathways and treatments? Am J Cardiol, 96(12B), 13M–18M.Find this resource:

Hatzimouratidis K, Hatzichristou DG (2005). A comparative review of the options for treatment of erectile dysfunction: which treatment for which patient? Drugs, 65, 1621–50.Find this resource:

Hauck EW, et al. (2006). A critical analysis of nonsurgical treatment of Peyronie’s disease. Eur Urol, 49, 987–97.Find this resource:

Johannes CB, et al. (2000). Incidence of erectile dysfunction in men 40 to 69 years old: longitudinal results from the Massachusetts male aging study. J Urol, 163, 460–3.Find this resource:

Kostis JB, et al. (2005). Sexual dysfunction and cardiac risk (the Second Princeton Consensus Conference). Am J Cardiol, 96, 313–21.Find this resource:

McMahon CN, Smith CJ, Shabsigh R (2006). Treating erectile dysfunction when PDE5 inhibitors fail. BMJ, 332, 589–92.Find this resource:

Montorsi F, Salonia A (2006). Medical therapy for premature ejaculation. Lancet, 368, 894–896.Find this resource:

Padma-Nathan H, et al. (2004). Pharmacotherapy for erectile dysfunction. J Sex Med, 1, 128–40.Find this resource:

Patrick DL, et al. (2005). Premature ejaculation: An observational study of men and their partners. J Sex Med, 2, 358–67.Find this resource:

Pryor J, et al. (2004). Peyronie’s disease. J Sex Med, 1, 110–15.Find this resource:

Pryor J, et al. (2004). Priapism. J Sex Med, 1, 116–20.Find this resource:

Rogers ZR (2005). Priapism in sickle cell disease. Hematol Oncol Clin North Am, 19, 917–28.Find this resource:

Travison TG, et al. (2007). The natural progression and remission of erectile dysfunction: results from the Massachusetts Male Aging Study. J Urol, 177, 241–6.Find this resource:

Wespes E, et al. (2006). EAU Guidelines on erectile dysfunction: an update. Eur Urol, 49, 806–15.Find this resource:

Female sexual dysfunction

Basson R (2002). The complexities of female sexual arousal disorder: potential role of pharmacotherapy. World J Urol, 20(2), 119–26.Find this resource:

Basson R, et al. (2004). Women’s sexual desire and arousal disorders and sexual pain. In: Lue TF, et al. (eds) Sexual medicine: sexual dysfunctions in men and women: 2nd International Consultation on Sexual Dysfunctions, pp. 851–974. Health Publications, Paris.Find this resource:

    Basson R, et al. (2004). Revised definitions of women’s sexual dysfunction. J Sex Med, 1, 40–8.Find this resource:

    Hatzichristou D, et al. (2004). Clinical evaluation and management strategy for sexual dysfunction in men and women. J Sex Med, 1, 49–57.Find this resource:

    Leiblum S, et al. (2005). Persistent sexual arousal syndrome: a descriptive study. J Sex Med, 2(3), 331–7.Find this resource:

    Meston CM, et al. (2004). Disorders of orgasm in women. J Sex Med, 1, 66–8.Find this resource:

    Segraves R, Woodard T (2006). Female hypoactive sexual desire disorder: History and current status. J Sex Med, 3, 408–18.Find this resource: