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.

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

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).

Meditation has demonstrated effectiveness in case studies.

There is yet no reliable medication for delayed ejaculation. PDE5 inhibitors such as Viagra have little effect. In fact, Viagra has a delaying effect on ejaculation, possibly through additional effect in the brain or decrease of sensitivity in the head of the penis.

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.

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.

Therapy usually involves homework assignments and exercises intended to help a man get used to having orgasms through insertional intercourse, vaginal, anal, or oral, that is through the way to which he is not accustomed. Commonly, the couple is advised to go through three stages. At the first stage, a man masturbates in the presence of his partner. Sometimes, this is not an easy matter as a man may be used to having orgasms alone. After a man learns to ejaculate in the presence of his partner, the man's hand is replaced with the hand of his partner. In the final stage, the receptive partner inserts the insertive partner's penis into the partner's vagina, anus, or mouth as soon as the ejaculation is felt to be imminent. Thus, a man gradually learns to ejaculate inside the desired orifice by an incremental process.

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.

Flibanserin is the first and only medication approved for women for the treatment of HSDD. It is only slightly effective over placebo, having been found to increase the average number of satisfying sexual events per month by 0.5 to 1. The side effects of dizziness, sleepiness, and nausea occur about three to four times more often. Overall improvement is slight to none.

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.

A few studies suggest that the antidepressant, bupropion, can improve sexual function in women who are not depressed, if they have HSDD. The same is true for the anxiolytic, buspirone, which is a 5-HT receptor agonist similarly to flibanserin.

Testosterone supplementation is effective in the short-term. However, its long-term safety is unclear.

Although erections are not necessary for satisfying sexual encounters, many men see them as important, and treating erectile dysfunction improves their relationships and quality of life. Whatever treatment is used, it works best in combination with talk-oriented therapy to help integrate it into the sex life.

Oral medications and mechanical devices are the first choice in treatment because they are less invasive, are often effective, and are well tolerated. Oral medications include sildenafil (Viagra), tadalafil (Cialis), and vardenafil (Levitra).

Penis pumps induce erections without the need for drugs or invasive treatments. To use a pump, the man inserts his penis into a cylinder, then pumps it to create a vacuum which draws blood into the penis, making it erect. He then slides a ring from the outside of the cylinder onto the base of the penis to hold the blood in and maintain the erection. A man who is able to get an erection but has trouble maintaining it for long enough can use a ring by itself. The ring cannot be left on for more than 30 minutes and cannot be used at the same time as anticoagulant medications.

If oral medications and mechanical treatments fail, the second choice is local injections: medications such as papaverine and prostaglandin that alter the blood flow and trigger erection are injected into the penis. This method is preferred for its effectiveness, but can cause pain and scarring.

Another option is to insert a small pellet of medication into the urethra, but this requires higher doses than injections and may not be as effective. Topical medications to dilate the blood vessels have been used, but are not very effective or well tolerated. Electrical stimulation of efferent nerves at the S2 level can be used to trigger an erection that lasts as long as the stimulation does.

Surgical implants, either of flexible rods or inflatable tubes, are reserved for when other methods fail because of the potential for serious complications, which occur in as many as 10% of cases. They carry the risk of eroding penile tissue (breaking through the skin). Although satisfaction among men who use them is high, if they do need to be removed implants make other methods such as injections and vacuum devices unusable due to tissue damage.

It is also possible for erectile dysfunction to exist not as a direct result of SCI but due to factors such as major depression, diabetes, or drugs such as those taken for spasticity. Finding and treating the root cause may alleviate the problem. For example, men who experience erectile problems as the result of a testosterone deficiency can receive androgen replacement therapy.

Compared with the options available for treating sexual dysfunction in men (for whom results are concretely observable), those available for women are limited. For example, PDE5 inhibitors, oral medications for treating erectile dysfunction in men, have been tested for their ability to increase sexual responses such as arousal and orgasm in women—but no controlled trials have been done in women with SCI, and trials in other women yielded only inconclusive results. In theory, women's sexual response could be improved using a vacuum device made to draw blood into the clitoris, but few studies on treatments for sexual function in women with SCI have been carried out. There is a particular paucity of information outside the area of reproduction.

Some drugs such as trazodone may cause priapism as a side effect, in which case discontinuing the medication may give relief. Additionally, the condition can sometimes start only after the discontinuation of SSRIs. In some recorded cases, the syndrome was caused by or can cause a pelvic arterial-venous malformation with arterial branches to the penis or clitoris; surgical treatment was effective in this case.

In other situations where the cause is unknown or less easily treatable, the symptoms can sometimes be reduced by the use of antidepressants, antiandrogenic agents, and anaesthetising gels. Psychotherapy with cognitive reframing of the arousal as a healthy response may also be used.

More recently, the symptoms of the condition have also been linked with pudendal nerve entrapment. Regional nerve blocks and less common surgical intervention have demonstrated varying degrees of success in most cases. There is, however, no evidence for the long-term efficacy of surgical intervention.

In one recent case, serendipitous relief of symptoms was noted from treatment with varenicline, a treatment for nicotine addiction.

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).

The FDA has approved one medication for the treatment of disorders of female libido, flibanserin.

Cognitive behavioral therapy is the mainstay of treatment. At other times counseling, anti-anxiety and antidepressant medications have been shown to be of use.

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.

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.

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.

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.

There is no standard method of treating or managing POIS. Patients need to be thoroughly examined in an attempt to find the causes of their POIS symptoms, which are often difficult to determine, and which vary across patients. Once a cause is hypothesized, an appropriate treatment can be attempted. At times, more than one treatment is attempted, until one that works is found.

Affected individuals typically avoid sexual activity, especially ejaculation, or schedule it for times when they can rest and recover for several days afterwards. In case post-coital tristesse (PCT) is suspected, patients could be treated with selective serotonin reuptake inhibitors.

Another patient, in whom POIS was suspected to be caused by cytokine release, was successfully treated with nonsteroidal anti-inflammatory drugs (NSAIDs) just prior to and for a day or two after ejaculation. The patient took diclofenac 75 mg 1 to 2 hours prior to sexual activity with orgasm, and continued twice daily for 24 to 48 hours.

One POIS patient with erectile dysfunction and premature ejaculation had much lower severity of symptoms on those occasions when he was able to maintain penile erection long enough to achieve vaginal penetration and ejaculate inside his partner. The patient took tadalafil to treat his erectile dysfunction and premature ejaculation. This increased the number of occasions on which he was able to ejaculate inside his partner, and decreased the number of occasions on which he experienced POIS symptoms. This patient is thought to have Dhat syndrome rather than true POIS.

In one patient, the POIS symptoms were so severe, that he decided to undergo castration in order to relieve them. The POIS symptoms were cured by the castration.

Two patients, in whom POIS was suspected to be caused by auto-immune reaction to their own semen, were successfully treated by allergen immunotherapy with their own autologous semen. They were given multiple subcutaneous injections of their own semen for three years. Treatment with autologous semen "might take 3 to 5 years before any clinically relevant symptom reduction would become manifest".

Treatments are not always successful, especially when the cause of POIS in a particular patient has not been determined. In one patient, all of whose routine laboratory tests were normal, the following were attempted, all without success: ibuprofen, 400 mg on demand; tramadol 50 mg one hour pre-coitally; and escitalopram 10 mg daily at bedtime for 3 months.

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.

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.