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

It can depend on one or more of several causes, including:

- Sexual inhibition

- Pharmacological inhibition. They include mostly antidepressant and antipsychotic medication, and the patients experiencing that tend to quit them

- Autonomic nervous system

- Prostatectomy - surgical removal of the prostate.

- Ejaculatory duct obstruction

- Spinal cord injury causes sexual dysfunction including anejaculation. The rate of being able to ejaculate varies with the type of lesion, as detailed in the table at right.

- old age

Anejaculation, especially the "orgasmic" variant, is usually indistinguishable from retrograde ejaculation. However, a negative urinalysis measuring no abnormal presence of spermatozoa in the urine will eliminate a retrograde ejaculation diagnosis.

Thus, if the affected man has the sensations and involuntary muscle-contractions of an orgasm but no or very low-volume semen, ejaculatory duct obstruction is another possible underlying pathology of anejaculation.

Medications to treat high blood pressure, benign prostate hyperplasia, mood disorders, surgery on the prostate and nerve injury (which may occur in multiple sclerosis, spinal cord injury or diabetes).

A malfunctioning bladder sphincter, leading to retrograde ejaculation, may be a result either of:

- Autonomic nervous system dysfunction. (Dysautonomia)

- Operation on the prostate. It is a common complication of transurethral resection of the prostate, a procedure in which prostate tissue is removed, slice by slice, through a resectoscope passed along the urethra.

It can also be caused by a retroperitoneal lymph node dissection for testicular cancer if nerve pathways to the bladder sphincter are damaged, with the resulting retrograde ejaculation being either temporary or permanent. Modern nerve-sparing techniques seek to reduce this risk; however, it may also occur as the result of Green Light Laser prostate surgery.

Surgery on the bladder neck accounted for about ten percent of the cases of retrograde ejaculation or anejaculation reported in a literature review.

Retrograde ejaculation is a common side effect of medications, such as tamsulosin, that are used to relax the muscles of the urinary tract, treating conditions such as benign prostatic hyperplasia. By relaxing the bladder sphincter muscle, the likelihood of retrograde ejaculation is increased.

The medications that mostly cause it are antidepressant and antipsychotic medication, as well as NRIs such as atomoxetine; patients experiencing this phenomenon tend to quit the medications.

Retrograde ejaculation can also be a complication of diabetes, especially in cases of diabetics with long term poor blood sugar control. This is due to neuropathy of the bladder sphincter. Post-pubertal males (aged 17 to 20 years) who experience repeated episodes of retrograde ejaculation are often diagnosed with urethral stricture disease shortly after the initial complaint arises. It is currently not known whether a congenital malformation of the bulbous urethra is responsible, or if pressure applied to the base of the penis or perineum immediately preceding ejaculatory inevitability may have inadvertently damaged the urethra. This damage is most often seen within 0.5 cm of the ejaculatory duct (usually distal to the duct).

Retrograde ejaculation can also result from pinching closed the urethral opening, to avoid creating a mess upon ejaculation (known as "Hughes' technique").

In posttesticular azoospermia sperm are produced but not ejaculated, a condition that affects 7–51% of azoospermic men. The main cause is a physical obstruction (obstructive azoospermia) of the posttesticular genital tracts. The most common reason is a vasectomy done to induce contraceptive sterility. Other obstructions can be congenital (example agenesis of the vas deferens as seen in certain cases of cystic fibrosis) or acquired, such as ejaculatory duct obstruction for instance by infection.

Ejaculatory disorders include retrograde ejaculation and anejaculation; in these conditions sperm are produced but not expelled.

In this situation the testes are abnormal, atrophic, or absent, and sperm production severely disturbed to absent. FSH levels tend to be elevated (hypergonadotropic) as the feedback loop is interrupted (lack of feedback inhibition on FSH). The condition is seen in 49–93% of men with azoospermia. Testicular failure includes absence of failure production as well as low production and maturation arrest during the process of spermatogenesis.

Causes for testicular failure include congenital issues such as in certain genetic conditions (e.g. Klinefelter syndrome), some cases of cryptorchidism or Sertoli cell-only syndrome as well as acquired conditions by infection (orchitis), surgery (trauma, cancer), radiation, or other causes. Mast cells releasing inflammatory mediators appear to directly suppress sperm motility in a potentially reversible manner, and may be a common pathophysiological mechanism for many causes leading to inflammation. Testicular azoospermia is a kind of non-obstructive azoospermia.

Generally, men with unexplained hypergonadotropic azoospermia need to undergo a chromosomal evaluation.

Although spinal cord injury (SCI) often causes sexual dysfunction, many people with SCI are able to have satisfying sex lives. Physical limitations acquired from SCI affect sexual function and sexuality in broader areas, which in turn has important effects on quality of life. Damage to the spinal cord impairs its ability to transmit messages between the brain and parts of the body below the level of the lesion. This results in lost or reduced sensation and muscle motion, and affects orgasm, erection, ejaculation, and vaginal lubrication. More indirect causes of sexual dysfunction include pain, weakness, and side effects of medications. Psycho-social causes include depression and altered self-image. Many people with SCI have satisfying sex lives, and many experience sexual arousal and orgasm. People with SCI employ a variety of adaptations to help carry on their sex lives healthily, by focusing on different areas of the body and types of sexual acts. Neural plasticity may account for increases in sensitivity in parts of the body that have not lost sensation, so people often find newly sensitive erotic areas of the skin in erogenous zones or near borders between areas of preserved and lost sensation.

Drugs, devices, surgery, and other interventions exist to help men achieve erection and ejaculation. Although male fertility is reduced, many men with SCI can still father children, particularly with medical interventions. Women's fertility is not usually affected, although precautions must be taken for safe pregnancy and delivery. People with SCI need to take measures during sexual activity to deal with SCI effects such as weakness and movement limitations, and to avoid injuries such as skin damage in areas of reduced sensation. Education and counseling about sexuality is an important part of SCI rehabilitation but is often missing or insufficient. Rehabilitation for children and adolescents aims to promote healthy development of sexuality and includes education for them and their families. Culturally inherited biases and stereotypes negatively affect people with SCI, particularly when held by professional caregivers. Body image and other insecurities affect sexual function, and have profound repercussions on self-esteem and self-concept. SCI causes difficulties in romantic partnerships, due to problems with sexual function and to other stresses introduced by the injury and disability, but many of those with SCI have fulfilling relationships and marriages. Relationships, self-esteem, and reproductive ability are all aspects of sexuality, which encompasses not just sexual practices but a complex array of factors: cultural, social, psychological, and emotional influences.

Low-volume, runny/fluid semen (oligospermia) or no semen at all (dry ejaculation/aspermia) are a logical consequence of an obstruction downstream of the seminal vesicles which contribute most to the volume of the semen. Usually, men will be able to observe a runny/fluid, low-volume semen by themselves during masturbation. Since the seminal vesicles contain a viscous, alkaline fluid rich in fructose, a chemical analysis of the semen of affected men will result in a low concentration of fructose and a low pH. A microscopic semen analysis will reveal aspermia/azoospermia.

In contrast, if both vasa deferentia are obstructed (which may be the result of intended sterilization), a semen analysis will also reveal aspermia/azoospermia, but an almost normal volume of the semen, since the efflux of the seminal vesicles is not hindered. This is because approx. 80% of the volume of the semen is the gel-like fluid originating from the seminal vesicles whereas the fraction from the testicles / epididymis, which contains the spermatozoa accounts for only 5–10% of the volume of the semen. In addition, if an obstruction of the vasa deferentia is the cause for the azoospermia, the concentration of fructose in the semen will also be normal, since the fructose comes primarily from the fluid stored in the seminal vesicles. If the seminal-vesicles contain spermatozoa, but the semen does not, the obstruction must be downstream of the seminal vesicles and the ejaculatory ducts are very likely to be obstructed, provided that other causes for a dry ejaculation/aspermia such as an retrograde ejaculation are ruled out.

Attempts are sometimes made to diagnose an ejaculatory duct obstruction by means of medical imaging, e.g. transrectal ultrasound or MRI, or by transrectal needle-aspiration of the seminal vesicles. However transrectal ultrasound has a relatively low sensitivity of approx. 50% and thus is only a tool to rule-out cysts in the region of the orifices but is not sufficient to rule out an obstruction of the ejaculatory ducts due to other causes. In approx. 50% of cases of unexplained low-volume azoospermia MRI and TRUS do not reveal any pathological findings, because it is difficult to see alterations in a narrowed, scarred duct with these methods. Due to the blockage of ejaculatory ducts, enlarged seminal vesicles are frequently seen in patients with ejaculatory duct obstructions. However, this is again neither a proof of an obstruction nor do normal-sized seminal vesicles rule-out an obstruction of the ejaculatory ducts. Since ejaculatory duct obstruction is a relatively rare cause of infertility, this possibility may be unfamiliar to some physicians, even some urologists.

The numbers of women with SCI giving birth and having healthy babies are increasing. Around a half to two-thirds of women with SCI report they might want to have children, and 14–20% do get pregnant at least once. Although female fertility is not usually permanently reduced by SCI, there is a stress response that can happen immediately post-injury that alters levels of fertility-related hormones in the body. In about half of women, menstruation stops after the injury but then returns within an average of five months—it returns within a year for a large majority. After menstruation returns, women with SCI become pregnant at a rate close to that of the rest of the population.

Pregnancy is associated with greater-than-normal risks in women with SCI, among them increased risk of deep vein thrombosis, respiratory infection, and urinary tract infection. Considerations exist such as maintaining proper positioning in a wheelchair, prevention of pressure sores, and increased difficulty moving due to weight gain and changes in center of balance. Assistive devices may need to be altered and medications changed.

For women with injuries above T6, a risk during labor and delivery that threatens both mother and fetus is autonomic dysreflexia, in which the blood pressure increases to dangerous levels high enough to cause potentially deadly stroke. Drugs such as nifedipine and captopril can be used to manage an episode if it occurs, and epidural anesthesia helps although it is not very reliable in women with SCI. Anesthesia is used for labor and delivery even for women without sensation, who may only experience contractions as abdominal discomfort, increased spasticity, and episodes of autonomic dysreflexia. Reduced sensation in the pelvic area means women with SCI usually have less painful delivery; in fact, they may fail to realize when they go into labor. If there are deformities in the pelvis or spine caesarian section may be necessary. Babies of women with SCI are more likely to be born prematurely, and, premature or not, they are more likely to be small for their gestational time.

If both ejaculatory ducts are completely obstructed, affected men will demonstrate male infertility due to aspermia/azoospermia. They will suffer from a very low volume of semen which lacks the gel-like fluid of the seminal vesicles or from no semen at all while they are able to have the sensation of an orgasm during which they will have involuntary contractions of the pelvic musculature. This is contrary to some other forms of anejaculation.

Ejaculatory duct obstruction is the underlying cause for 1–5% of male infertility.

In addition, it is reported to be a cause for pelvic pain, especially shortly after ejaculation. In case of proven fertility but unresolved pelvic pain, even one or both partially obstructed ejaculatory ducts may be the origin of pelvic pain and oligospermia.

Ejaculatory duct obstruction may result in a complete lack of semen (aspermia) or a very low-volume semen (oligospermia) which may contain only the secretion of accessory prostate glands downstream to the orifice of the ejaculatory ducts.

In addition to the congenital form which is often caused by cysts of the müllerian duct the obstruction can be acquired due to an inflammation caused by chlamydia, prostatitis, tuberculosis of the prostate and other pathogens. In Addition, calculus was reported to mechanically block the ejaculatory duct, leading to infertility. However, in many patients, there is no history of an inflammation and the underlying cause simply remains unknown.

A supplemental system of phenotypic grading that uses seven classes instead of the traditional three was proposed by pediatric endocrinologist Charmian A. Quigley et al. in 1995. The first six grades of the scale, grades 1 through 6, are differentiated by the degree of genital masculinization; grade 1 is indicated when the external genitalia is fully masculinized, grade 6 is indicated when the external genitalia is fully feminized, and grades 2 through 5 quantify four degrees of increasingly feminized genitalia that lie in the interim. Grade 7 is indistinguishable from grade 6 until puberty, and is thereafter differentiated by the presence of secondary terminal hair; grade 6 is indicated when secondary terminal hair is present, whereas grade 7 is indicated when it is absent. The Quigley scale can be used in conjunction with the traditional three classes of AIS to provide additional information regarding the degree of genital masculinization, and is particularly useful when the diagnosis is PAIS.

Partial androgen insensitivity syndrome is diagnosed when the degree of androgen insensitivity in an individual with a 46,XY karyotype is great enough to partially prevent the masculinization of the genitalia, but is not great enough to completely prevent genital masculinization. This includes any phenotype resulting from androgen insensitivity where the genitalia is partially, but not completely masculinized. Genital ambiguities are frequently detected during clinical examination at birth, and consequently, a PAIS diagnosis can be made during infancy as part of a differential diagnostic workup.

Pubertal undervirilization is common, including gynecomastia, decreased secondary terminal hair, and / or a high pitched voice. The phallic structure ranges from a penis with varying degrees of diminished size and hypospadias to a slightly enlarged clitoris. Wolffian structures (the epididymides, vasa deferentia, and seminal vesicles) are typically partially or fully developed. The prostate is typically small or impalpable. Müllerian remnants are rare, but have been reported.

The gonads in individuals with PAIS are testes, regardless of phenotype; during the embryonic stage of development, testes form in an androgen-independent process that occurs due to the influence of the SRY gene on the Y chromosome. Cryptorchidism is common, and carries with it a 50% risk of germ cell malignancy. If the testes are located intrascrotally, there may still be significant risk of germ cell malignancy; studies have not yet been published to assess this risk.

Predominantly male phenotypes vary in the degree of genital undermasculinization to include micropenis, chordee, scrotum, and / or pseudovaginal perineoscrotal hypospadias. Impotence may be fairly common, depending on phenotypic features; in one study of 15 males with PAIS, 80% of those interviewed indicated that they had some degree of impotence. Anejaculation appears to occur somewhat independently of impotence; some men are still able to ejaculate despite impotence, and others without erectile difficulties cannot. Predominantly female phenotypes include a variable degree of labial fusion and clitoromegaly. Ambiguous phenotypic states include a phallic structure that is intermediate between a clitoris and a penis, and a single perineal orifice that connects to both the urethra and the vagina (i.e. urogenital sinus). At birth, it may not be possible to immediately differentiate the external genitalia of individuals with PAIS as being either male or female, although the majority of individuals with PAIS are raised male.

Given the wide diversity of phenotypes associated with PAIS, the diagnosis is often further specified by assessing genital masculinization. Grades 2 through 5 of the Quigley scale quantify four degrees of increasingly feminized genitalia that correspond to PAIS.

Grade 2, the mildest form of PAIS, presents with a predominantly male phenotype that presents with minor signs of undermasculinized genitalia, such as isolated hypospadias, which can be severe. Hypospadias may manifest with a partially formed channel from the urethral opening to the glans. Until recently, it was thought that isolated micropenis was not a manifestation of PAIS. However, in 2010, two cases of PAIS manifesting with isolated micropenis were documented.

Grade 3, the most common phenotypic form of PAIS, features a predominantly male phenotype that is more severely undermasculinized, and typically presents with micropenis and pseudovaginal perineoscrotal hypospadias with scrotum.

Grade 4 presents with a gender ambiguous phenotype, including a phallic structure that is intermediate between a clitoris and a penis. The urethra typically opens into a common channel with the vagina (i.e. urogenital sinus).

Grade 5, the form of PAIS with the greatest degree of androgen insensitivity, presents with a mostly female phenotype, including separate urethral and vaginal orifices, but also shows signs of slight masculinization including mild clitoromegaly and / or partial labial fusion.

Previously, it was erroneously thought that individuals with PAIS were always infertile; at least one case report has been published that describes fertile men that fit the criteria for grade 2 PAIS (micropenis, penile hypospadias, and gynecomastia).

All forms of androgen insensitivity are associated with infertility, though exceptions have been reported for both the mild and partial forms.

PAIS is associated with a 50% risk of germ cell malignancy when the testes are undescended. If the testes are located intrascrotally, there may still be significant risk of germ cell malignancy; studies have not yet been published to assess this risk. Some men with PAIS may experience sexual dysfunction including impotence and anejaculation. A few AR mutations that cause PAIS are also associated with prostate and breast cancers.

Vaginal hypoplasia, a relatively frequent finding in CAIS and some forms of PAIS, is associated with sexual difficulties including vaginal penetration difficulties and dyspareunia.

At least one study indicates that individuals with an intersex condition may be more prone to psychological difficulties, due at least in part to parental attitudes and behaviors, and concludes that preventative long-term psychological counseling for parents as well as for affected individuals should be initiated at the time of diagnosis.

Lifespan is not thought to be affected by AIS.