The treatment depends on the cause. Medications may work for retrograde ejaculation but only in a few cases. Surgery rarely is the first option for retrograde ejaculation and the results have proven to be inconsistent. Medications do not help retrograde ejaculation if there has been permanent damage to the prostate or the testes from radiation. Medications also do not help if prostate surgery has resulted in damage to the muscles or nerves. Medications only work if there has been mild nerve damage caused by diabetes, multiple sclerosis or mild spinal cord injury.

The PDE5 inhibitors sildenafil (Viagra), vardenafil (Levitra) and tadalafil (Cialis) are prescription drugs which are taken orally.

A cream combining alprostadil with the permeation enhancer DDAIP has been approved in Canada as a first line treatment for erectile dysfunction.

One of the following medications maybe injected into the penis: papaverine, phentolamine, and prostaglandin E1.

These medications tighten the bladder neck muscles and prevent semen from going backwards into the bladder. However, the medications do have many side effects and they have to be taken at least 1–2 hours prior to sexual intercourse. In many cases, the medications fail to work at the right time because most men are not able to predict when they will have an orgasm.

Treatment depends on the cause.

Exercise, particularly aerobic exercise during midlife is effective for preventing ED; exercise as a treatment is under investigation. For tobacco smokers, cessation results in a significant improvement.

Oral pharmacotherapy and vacuum erection devices are first-line treatments, followed by injections of drugs into the penis, and penile implants.

Just as with erectile dysfunction in men, lack of sexual function in women may be treated with hormonal patches or tablets to correct hormonal imbalances, clitoral vacuum pump devices and medication to improve blood flow, sexual sensation and arousal.

Many practitioners today treat both men and women who have SSRI-induced anorgasmia with sildenafil, more commonly known as Viagra. While this approach is known to work well in men with sexual dysfunction, it is only recently that the effectiveness of sildenafil in women with sexual dysfunction is coming to light. A recent study by H. G. Nurnberg et al. showed a complete or very significant reversal of their sexual dysfunction upon taking sildenafil one hour prior to sexual activity. In this study, eight out of the nine women required 50 mg of sildenafil while the 9th woman required 100 mg of sildenafil.

Another option for women who have SSRI-induced anorgasmia is the use of vardenafil. Vardenafil is a type 5 phosphodiesterase (PDE5) inhibitor that facilitates muscle relaxation and improves penile erection in men. However, there is much controversy about the efficiency of the drug used in the reversal of female sexual dysfunction. Vardenafil is similar to sildenafil, but vardenafil is less expensive and may be covered under some insurance plans. A study by A.K. Ashton M.D. has shown that in the case of one particular woman, the effects of vardenafil as opposed to sildenafil have not only been comparable in the effectiveness, but that vardenafil is cheaper and reversal of sexual dysfunction requires a smaller dose. So far, vardenafil has been approved by the Food and Drug administration only for use in men.

The NIH states that yohimbine hydrochloride has been shown in human studies to be possibly effective in the treatment of male impotence resulting from erectile dysfunction or SSRI usage (e.g., anorgasmia). Published reports have shown it to be effective in the treatment of orgasmic dysfunction in men.

Cabergoline, an agonist of dopamine D₂ receptors which inhibits prolactin production, was found in a small study to fully restore orgasm in one third of anorgasmic subjects, and partially restore orgasm in another third. Limited data has shown that the drug amantadine may help to relieve SSRI-induced sexual dysfunction. Cyproheptadine, buspirone, stimulants such as amphetamines (including the antidepressant bupropion), nefazodone and yohimbine have been used to treat SSRI-induced anorgasmia. Reducing the SSRI dosage may also resolve anorgasmia problems.

A method to treat ejaculatory duct obstruction is transurethral resection of the ejaculatory ducts (TURED). This operative procedure is relatively invasive, has some severe complications, and has led to natural pregnancies of their partners in approximately 20% of affected men. A disadvantage is the destruction of the valves at the openings of the ejaculatory ducts into the urethra such that urine may flow backwards into the seminal vesicles. Another, experimental approach is the recanalization of the ejaculatory ducts by transrectal or transurethral inserted balloon catheter. Though much less invasive and preserving the anatomy of the ejaculatory ducts, this procedure is probably not completely free of complications either and success rates are unknown. There is a clinical study currently ongoing to examine the success rate of recanalization of the ejaculatory ducts by means of balloon dilation.

Usually, affected men have a normal production of spermatozoa in their testicles, so that after spermatozoa were harvested directly from the testes e.g. by TESE, or the seminal vesicles (by needle aspiration) they and their partners are potentially candidates for some treatment options of assisted reproduction e.g. in-vitro fertilisation. Note that in this case, most of the treatment (e.g. ovarian stimulation and transvaginal oocyte retrieval) is transferred to the female partner.

Drugs that increase serotonin signalling in the brain slow ejaculation and have been used successfully to treat PE. These include selective serotonin reuptake inhibitors (SSRIs), such as paroxetine or dapoxetine, as well as clomipramine. Ejaculatory delay typically begins within a week of beginning medication. The treatments increase the ejaculatory delay to 6–20 times greater than before medication. Men often report satisfaction with treatment by medication, and many discontinue it within a year. However, SSRIs can cause various types of sexual dysfunction such as anorgasmia, erectile dysfunction, and diminished libido.

Dapoxetine is a short-acting SSRI which appears to work when taken as needed for PE. It is generally well tolerated. Tramadol, an atypical oral analgesic, appears to be effective.

Desensitizing topical medications like lidocaine that are applied to the tip and shaft of the penis can also be used. These are applied "as needed", 10–15 minutes before sexual activity and have fewer potential systemic side effects as compared to pills. Use of topicals is sometimes disliked due to the reduction of sensation in the penis as well as for the partner (due to the medication rubbing onto the partner).

Several treatments have been tested for treating premature ejaculation. A combination of medication and non-medication treatments is often the most effective method.

Although there are no approved pharmaceuticals for addressing female sexual disorders, several are under investigation for their effectiveness. A vacuum device is the only approved medical device for arousal and orgasm disorders. It is designed to increase blood flow to the clitoris and external genitalia. Women experiencing pain with intercourse are often prescribed pain relievers or desensitizing agents. Others are prescribed lubricants and/or hormone therapy. Many patients with female sexual dysfunction are often also referred to a counselor or therapist for psychosocial counseling.

The first-line method for sperm retrieval in men with spinal cord injury is "penile vibratory stimulation" (PVS). The penile vibratory stimulator is a plier-like device that is placed around glans penis to stimulate it by vibration. In case of failure with PVS, spermatozoa are sometimes collected by electroejaculation, or surgically by per cutaneous epididymal sperm aspiration (PESA) or testicular sperm extraction (TESE).

Estrogens are responsible for the maintenance of collagen, elastic fibers, and vasoculature of the urogenital tract, all of which are important in maintaining vaginal structure and functional integrity; they are also important for maintaining vaginal pH and moisture levels, both of which aid in keeping the tissues lubricated and protected. Prolonged estrogen deficiency leads to atrophy, fibrosis, and reduced blood flow to the urogenital tract, which is what causes menopausal symptoms such as vaginal dryness and pain related to sexual activity and/or intercourse. It has been consistently demonstrated that women with lower sexual functioning have lower estradiol levels.

Androgen therapy for hypoactive sexual desire disorder (HSDD) has a small benefit but its safety is not known. It is not approved as a treatment in the United States. If used it is more common among women who have had an oophorectomy or who are in a postmenopausal state. However, like most treatments, this is also controversial. One study found that after a 24-week trial, those women taking androgens had higher scores of sexual desire compared to a placebo group. As with all pharmacological drugs, there are side effects in using androgens, which include hirutism, acne, ploycythaemia, increased high-density lipoproteins, cardiovascular risks, and endometrial hyperplasia is a possibility in women without hysterectomy. Alternative treatments include topical estrogen creams and gels can be applied to the vulva or vagina area to treat vaginal dryness and atrophy.

The 5α-reductase inhibitors finasteride and dutasteride may also be used in men with BPH. These medications inhibit the 5α-reductase enzyme, which, in turn, inhibits production of DHT, a hormone responsible for enlarging the prostate. Effects may take longer to appear than alpha blockers, but they persist for many years. When used together with alpha blockers, no benefit was reported in short-term trials, but in a longer term study (3–4 years) there was a greater reduction in BPH progression to acute urinary retention and surgery than with either agent alone, especially in patients were more severe symptoms and larger prostates. Other trials have confirmed reductions in symptoms, within 6 months in one trial, an effect that was maintained after withdrawal of the alpha blocker. Side effects include decreased libido and ejaculatory or erectile dysfunction. The 5α-reductase inhibitors are contraindicated in pregnant women because of their teratogenicity due to interference with fetal testosterone metabolism, and as a precaution, pregnant women should not handle crushed or broken tablets.

Selective α-blockers are the most common choice for initial therapy. They include alfuzosin, doxazosin, silodosin, tamsulosin, and terazosin. They have a small to moderate benefit. All five are equally effective but have slightly different side effect profiles. Alpha blockers relax smooth muscle in the prostate and the bladder neck, thus decreasing the blockage of urine flow. Common side effects of alpha blockers include orthostatic hypotension (a head rush or dizzy spell when standing up or stretching), ejaculation changes, erectile dysfunction, headaches, nasal congestion, and weakness.

Tamsulosin and silodosin are selective α1 receptor blockers that preferentially bind to the α1A receptor in the prostate instead of the α1B receptor in the blood vessels. Less-selective α1 receptor blockers such as terazosin and doxazosin may lower blood pressure. The older, less selective α1-adrenergic blocker prazosin is not a first line choice for either high blood pressure or prostatic hyperplasia; it is a choice for patients who present with both problems at the same time. The older, broadly non-selective alpha blocker medications such as phenoxybenzamine are not recommended for control of BPH. Non-selective alpha blockers such as terazosin and doxazosin may also require slow dose adjustments as they can lower blood pressure and cause syncope (fainting) if the response to the medication is too strong.

Treatments vary according to the underlying disease and the degree of the impairment of the male fertility. Further, in an infertility situation, the fertility of the female needs to be considered.

Pre-testicular conditions can often be addressed by medical means or interventions.

Testicular-based male infertility tends to be resistant to medication. Usual approaches include using the sperm for intrauterine insemination (IUI), in vitro fertilization (IVF), or IVF with intracytoplasmatic sperm injection (ICSI). With IVF-ICSI even with a few sperm pregnancies can be achieved.

Obstructive causes of post-testicular infertility can be overcome with either surgery or IVF-ICSI. Ejaculatory factors may be treatable by medication, or by IUI therapy or IVF.

Vitamin E helps counter oxidative stress, which is associated with sperm DNA damage and reduced sperm motility. A hormone-antioxidant combination may improve sperm count and motility. However there is only some low quality evidence from few small studies that oral antioxidants given to males in couples undergoing in vitro fertilisation for male factor or unexplained subfertility result in higher live birth rate. It is unclear if there are any adverse effects.

Administration of luteinizing hormone (LH) (or human chorionic gonadotropin) and follicle-stimulating hormone (FSH) is very effective in the treatment of male infertility due to hypogonadotropic hypogonadism. Although controversial, off-label clomiphene citrate, an antiestrogen, may also be effective by elevating gonadotropin levels.

Though androgens are absolutely essential for spermatogenesis and therefore male fertility, exogenous testosterone therapy has been found to be ineffective in benefiting men with low sperm count. This is thought to be because very high local levels of testosterone in the testes (concentrations in the seminiferous tubules are 20- to 100-fold greater than circulating levels) are required to mediate spermatogenesis, and exogenous testosterone therapy (which is administered systemically) cannot achieve these required high local concentrations (at least not without extremely supraphysiological dosages). Moreover, exogenous androgen therapy can actually impair or abolish male fertility by suppressing gonadotropin secretion from the pituitary gland, as seen in users of androgens/anabolic steroids (who often have partially or completely suppressed sperm production). This is because suppression of gonadotropin levels results in decreased testicular androgen production (causing diminished local concentrations in the testes) and because FSH is independently critical for spermatogenesis. In contrast to FSH, LH has little role in male fertility outside of inducing gonadal testosterone production.

Estrogen, at some concentration, has been found to be essential for male fertility/spermatogenesis. However, estrogen levels that are too high can impair male fertility by suppressing gonadotropin secretion and thereby diminishing intratesticular androgen levels. As such, clomiphene citrate (an antiestrogen) and aromatase inhibitors such as testolactone or anastrozole have shown effectiveness in benefiting spermatogenesis.

Low-dose estrogen and testosterone combination therapy may improve sperm count and motility in some men, including in men with severe oligospermia.

Treatment takes place within the context of infertility management and needs also to consider the fecundity of the female partner. Thus the choices can be complex.

In a number of situations direct medical or surgical intervention can improve the sperm concentration, examples are use of FSH in men with pituitary hypogonadism, antibiotics in case of infections, or operative corrections of a hydrocele, varicocele, or vas deferens obstruction.

In most cases of oligospermia including its idiopathic form there is no direct medical or surgical intervention agreed to be effective. Empirically many medical approaches have been tried including clomiphene citrate, tamoxifen, HMG, FSH, HCG, testosterone, Vitamin E, Vitamin C, anti-oxidants, carnitine, acetyl-L-carnitine, zinc, high-protein diets. In a number of pilot studies some positive results have been obtained. Clomiphene citrate has been used with modest success. The combination of tamoxifen plus testosterone was reported to improve the sperm situation.

The use of carnitine showed some promise in a controlled trial in selected cases of male infertility improving sperm quality and further studies are needed.

In many situations, intrauterine inseminations are performed with success. In more severe cases IVF, or IVF - ICSI is done and is often the best option, specifically if time is a factor or fertility problems coexist on the female side.

The Low dose Estrogen Testosterone Combination Therapy may improve sperm count and motility in some men including severe oligospermia.

Pre- and post-testicular azoospermia are frequently correctible, while testicular azoospermia is usually permanent. In the former the cause of the azoospermia needs to be considered and it opens up possibilities to manage this situation directly. Thus men with azoospermia due to hyperprolactinemia may resume sperm production after treatment of hyperprolactinemia or men whose sperm production is suppressed by exogenous androgens are expected to produce sperm after cessation of androgen intake. In situations where the testes are normal but unstimulated, gonadotropin therapy can be expected to induce sperm production.

A major advancement in recent years has been the introduction of IVF with ICSI which allows successful fertilization even with immature sperm or sperm obtained directly from testicular tissue. IVF-ICSI allows for pregnancy in couples where the man has irreversible testicular azoospermia as long as it is possible to recover sperm material from the testes. Thus men with non-mosaic Klinefelter's syndrome have fathered children using IVF-ICSI. Pregnancies have been achieved in situations where azoospermia was associated with cryptorchism and sperm where obtained by testicular sperm extraction (TESE).

In men with posttesticular azoospermia a number of approaches are available. For obstructive azoospermia IVF-ICSI or surgery can be used and individual factors need to be considered for the choice of treatment. Medication may be helpful for retrograde ejaculation.

Achieving a pregnancy naturally may be a challenge if the male suffers from a low sperm count. However, chances are good if the female partner is fertile; many couples with this problem have been successful. Prognosis is more limited if there is a combination of factors that include sperm dysfunction and reduced ovarian reserve.

A number of medications can be used to treat this disorder. Alpha blockers and/or antibiotics appear to be the most effective with NSAIDs such as ibuprofen providing lesser benefit.

- Treatment with antibiotics is controversial. Some have found benefits in symptoms while others have questioned the utility of a trial of antibiotics. Antibiotics are known to have anti-inflammatory properties and this has been suggested as an explanation for their partial efficacy in treating CPPS. Antibiotics such as fluoroquinolones, tetracyclines, and macrolides have direct anti-inflammatory properties in the absence of infection, blocking inflammatory chemical signals (cytokines) such as interleukin-1 (IL-1), interleukin-8 and tumor necrosis factor (TNF), which coincidentally are the same cytokines found to be elevated in the semen and EPS of men with chronic prostatitis.

- The effectiveness of alpha blockers (tamsulosin, alfuzosin) is questionable in men with CPPS. A 2006 meta-analysis found that they are moderately beneficial when the duration of therapy was at least 3 months.

- An estrogen reabsorption inhibitor such as mepartricin improves voiding, reduces urological pain and improves quality of life in patients with chronic non-bacterial prostatitis.

- Therapies that have not been properly evaluated in clinical trials although there is supportive anecdotal evidence include gabapentin, benzodiazepines, and amitriptyline.

Transurethral needle ablation of the prostate (TUNA) has been shown to be ineffective in trials.

Anejaculation is the pathological inability to ejaculate in males, with ("orgasmic") or without ("anorgasmic") orgasm.

In both the acute and chronic forms, antibiotics are used if an infection is suspected. The treatment of choice is often azithromycin and cefixime to cover both gonorrhoeae and chlamydia. Fluoroquinolones are no longer recommended due to widespread resistance of gonorrhoeae to this class. Doxycycline may be used as an alternative to azithromycin. In chronic epididymitis, a four- to six-week course of antibiotics may be prescribed to ensure the complete eradication of any possible bacterial cause, especially the various chlamydiae.

For cases caused by enteric organisms (such as "E. coli"), ofloxacin or levofloxacin are recommended.

In children, fluoroquinolones and doxycycline are best avoided. Since bacteria that cause urinary tract infections are often the cause of epididymitis in children, co-trimoxazole or suited penicillins (for example, cephalexin) can be used.

Household remedies such as elevation of the scrotum and cold compresses applied regularly to the scrotum may relieve the pain in acute cases. Painkillers or anti-inflammatory drugs are often used for treatment of both chronic and acute forms. Hospitalisation is indicated for severe cases, and check-ups can ensure the infection has cleared up. Surgical removal of the epididymis is rarely necessary, causes sterility, and only gives relief from pain in approximately 50% of cases. However, in acute suppurating epididymitis (acute epididymitis with a discharge of pus), a epididymotomy may be recommended; in refractory cases, a full epididymectomy may be required. In cases with unrelenting testicular pain, removal of the entire testicle—orchiectomy—may also be warranted.

It is generally believed that most cases of chronic epididymitis will eventually "burn out" of patient's system if left untreated, though this might take years or even decades. However, some prostate-related medications have proven effective in treating chronic epididymitis, including doxazosin.

Cystoceles are treated with a surgical procedure known as a Burch colposuspension, with the goal of suspending the prolapsed urethra so that the urethrovesical junction and proximal urethra are replaced in the pelvic cavity. Uteroceles are treated with hysterectomy and uterosacral suspension. With enteroceles, the prolapsed small bowel is elevated into the pelvis cavity and the rectovaginal fascia is reapproximated. Rectoceles, in which the anterior wall of the rectum protrudes into the posterior wall of the vagina, require posterior colporrhaphy.

The condition is widespread, affecting up to 50% of women at some point in their lifetime. Almost 10 percent of women will undergo surgery for urinary incontinence or pelvic organ prolapse. 30 percent of those undergoing surgery will have at least two surgeries in trying to correct the problem.

Some conditions are reversible, with pelvic floor exercises, or Kegel exercises recommended to strengthen the area muscles. Devices and probes are also available over the counter which purport to increase pelvic floor tone by stimulating muscle contractions with electrical impulses.

The condition is sometimes classified as a psychiatric disorder. However, it can also be caused by medical problems such as diabetic neuropathy, multiple sclerosis, genital mutilation, complications from genital surgery, pelvic trauma (such as from a straddle injury caused by falling on the bars of a climbing frame, bicycle or gymnastics beam), hormonal imbalances, total hysterectomy, spinal cord injury, cauda equina syndrome, uterine embolisation, childbirth trauma (vaginal tearing through the use of forceps or suction or a large or unclosed episiotomy), vulvodynia and cardiovascular disease.

A common cause of situational anorgasmia, in both men and women, is the use of anti-depressants, particularly selective serotonin reuptake inhibitors (SSRIs). Though reporting of anorgasmia as a side effect of SSRIs is not precise, studies have found that 17–41% of users of such medications are affected by some form of sexual dysfunction.

Another cause of anorgasmia is opiate addiction, particularly to heroin.

About 15% of women report difficulties with orgasm, and as many as 10% of women in the United States have never climaxed. Only 29% of women always have orgasms with their partner.