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Orgasm and Ejaculation Disorders (2022)
Federico Belladelli, Edoardo Pozzi, Giuseppe Fallara, Paolo Capogrosso, and Andrea Salonia
7.1 Anatomy and Physiology of Orgasm and Ejaculation
There is no standard definition of orgasm, although it has been defined as an intense transient peak sensation of pleasure alternating the state of consciousness and associated with reported physical changes. It is commonly combined with ejaculation [1] although the experience of orgasm is a distinct cortical event, associated with the perception of striated muscle contractions and resulting in semen expelled during ejaculation, mediated through sensory neurons in the pelvic region. During orgasm, hyperventilation of up to 40 breaths/ min, tachycardia, and high blood pressure could occur [1]. Both ejaculation and orgasm are based on a complex interplay between the central nervous system and the peripheral nervous system, with the involvement of several neurotransmitters, thus including dopamine, norepinephrine, serotonin, acetylcholine, gamma-aminobutyric acid (GABA), and nitric oxide (NO) [2]; moreover, hormonal pathways may influence the process of ejaculation with an active role played by oxytocin, prolactin, thyroid hormones, glucocorticoids, and sex steroid hormones [2]. Different studies using positron emission tomography (PET) have identified areas of activation in the brain during orgasm. Primary intense activation areas are noted to be in the mesodiencephalic transition zones, which include the midline, the zona incerta, ventroposterior and intralaminar thalamic nuclei, the lateral segmental central field, the suprafascicular nucleus, the ventral tegmental area. Strong increases were seen in the cerebellum. Decreases were noted at the entorhinal cortex and the amygdala [3]. In men, a period of inhibition normally follows orgasm, called the refractory period. This is a poorly understood phenomenon, with some investigators suggesting a central rather than spinal mechanism to be involved [4].
Ejaculation is a different physiological process mainly under the regulation of the autonomic nervous system. It consists of two main phases: emission and expulsion. The first step in the emission phase is the closure of the bladder neck to prevent retrograde spillage of the seminal fluid into the bladder. This is followed by the ejection of prostatic secretions, mixed with spermatozoa from the vas deferens into the prostatic urethra [5]. The organs involved in the ejaculation process receive dense autonomic nerve supply, both sympathetic and parasympathetic, from the pelvic plexus. The sympathetic neurons play the predominant role in the ejaculation process. Input from genital stimulation is integrated at the neural sacral spinal level to produce emission [6]. The emission phase of ejaculation is also under considerable cerebral control and can be induced through physical or visual erotic stimulation [7]. Expulsion follows emission and refers to the ejection of semen through the urethral meatus. The semen is propelled through a number of rhythmic contractions of the pelvic striated muscles in addition to the bulbospongiosus and ischiocavernosus muscles [1]. To achieve antegrade semen expulsion, the bladder neck remains closed, whereas the external urethral sphincter is open.
7.2 Premature Ejaculation (PE)
7.2.1 Aetiology
7.2.1.1 Hereditary PE
7.2.1.2 Neurobiology of PE
7.2.1.3 Hormones and PE
7.2.1.4 Chronic Prostatitis and Chronic Pelvic Pain Syndrome (CPPS)
7.2.1.5 Psychological Factors
7.2.1.6 Pharmacology and PE
7.2.2 Diagnosis
7.2.2.1 History and Questionnaires
7.2.2.2 Physical Examination
7.2.3 Treatments
1. Selective Serotonin Reuptake Inhibitors (SSRIs)
2. Topical Anaesthetics
3. Psychotherapy
Other available treatments are as follows:
1. Phosphodiesterase type 5 inhibitors (PDE5i)
2. Topical Alprostadil cream (200/300 μg)
3. Tramadol
4. Alpha Blockers
7.3 Delayed Ejaculation (DE)
7.3.1 Aetiology
There are mainly three aetiological factors that are well-recognized in the context of DE [44].
1. Aging: degeneration of penile afferent nerves inhibits ejaculation.
2. Congenital: Mullerian duct cyst, Wolffian duct abnormalities, Prune Belly Syndrome, imperforate anus, and genetic abnormalities.
3. Anatomic causes: transurethral resection of the prostate, bladder neck incision, circumcision, and ejaculatory duct obstruction (can be congenital or acquired).
4. Neurogenic causes: diabetic autonomic neuropathy, multiple sclerosis, spinal cord injury, radical prostatectomy, proctocolectomy, bilateral sympathectomy, abdominal aortic aneurysmectomy, and para-aortic lymphadenectomy.
5. Infective/inflammatory causes: urethritis, genitourinary tuberculosis, schistosomiasis, prostatitis, and orchitis.
6. Endocrine causes: hypogonadism, hypothyroidism, and prolactin disorders.
7. Medications: antihypertensives, thiazide diuretics, alpha-adrenergic blockers, antipsychotics, antidepressants, alcohol, antiandrogens, ganglion blockers, and SSRIs. 8. Psychological: acute psychological distress, relationship distress, psychosexual skill deficit, disconnect between arousal and sexual situations masturbation style.
7.3.2 Diagnosis of DE
7.3.3 Treatment
1. Psychological support
2. Pharmacotherapy
3. Penile vibratory stimulation
7.4 Retrograde Ejaculation
7.4.1 Aetiology
7.4.2 Diagnosis of RE
7.4.3 Treatment
7.5 Anejaculation and Anorgasmia
7.5.1 Aetiology
7.5.2 Diagnosis
7.5.3 Treatment
Federico Belladelli, Edoardo Pozzi, Giuseppe Fallara, Paolo Capogrosso, and Andrea Salonia
7.1 Anatomy and Physiology of Orgasm and Ejaculation
There is no standard definition of orgasm, although it has been defined as an intense transient peak sensation of pleasure alternating the state of consciousness and associated with reported physical changes. It is commonly combined with ejaculation [1] although the experience of orgasm is a distinct cortical event, associated with the perception of striated muscle contractions and resulting in semen expelled during ejaculation, mediated through sensory neurons in the pelvic region. During orgasm, hyperventilation of up to 40 breaths/ min, tachycardia, and high blood pressure could occur [1]. Both ejaculation and orgasm are based on a complex interplay between the central nervous system and the peripheral nervous system, with the involvement of several neurotransmitters, thus including dopamine, norepinephrine, serotonin, acetylcholine, gamma-aminobutyric acid (GABA), and nitric oxide (NO) [2]; moreover, hormonal pathways may influence the process of ejaculation with an active role played by oxytocin, prolactin, thyroid hormones, glucocorticoids, and sex steroid hormones [2]. Different studies using positron emission tomography (PET) have identified areas of activation in the brain during orgasm. Primary intense activation areas are noted to be in the mesodiencephalic transition zones, which include the midline, the zona incerta, ventroposterior and intralaminar thalamic nuclei, the lateral segmental central field, the suprafascicular nucleus, the ventral tegmental area. Strong increases were seen in the cerebellum. Decreases were noted at the entorhinal cortex and the amygdala [3]. In men, a period of inhibition normally follows orgasm, called the refractory period. This is a poorly understood phenomenon, with some investigators suggesting a central rather than spinal mechanism to be involved [4].
Ejaculation is a different physiological process mainly under the regulation of the autonomic nervous system. It consists of two main phases: emission and expulsion. The first step in the emission phase is the closure of the bladder neck to prevent retrograde spillage of the seminal fluid into the bladder. This is followed by the ejection of prostatic secretions, mixed with spermatozoa from the vas deferens into the prostatic urethra [5]. The organs involved in the ejaculation process receive dense autonomic nerve supply, both sympathetic and parasympathetic, from the pelvic plexus. The sympathetic neurons play the predominant role in the ejaculation process. Input from genital stimulation is integrated at the neural sacral spinal level to produce emission [6]. The emission phase of ejaculation is also under considerable cerebral control and can be induced through physical or visual erotic stimulation [7]. Expulsion follows emission and refers to the ejection of semen through the urethral meatus. The semen is propelled through a number of rhythmic contractions of the pelvic striated muscles in addition to the bulbospongiosus and ischiocavernosus muscles [1]. To achieve antegrade semen expulsion, the bladder neck remains closed, whereas the external urethral sphincter is open.
7.2 Premature Ejaculation (PE)
7.2.1 Aetiology
7.2.1.1 Hereditary PE
7.2.1.2 Neurobiology of PE
7.2.1.3 Hormones and PE
7.2.1.4 Chronic Prostatitis and Chronic Pelvic Pain Syndrome (CPPS)
7.2.1.5 Psychological Factors
7.2.1.6 Pharmacology and PE
7.2.2 Diagnosis
7.2.2.1 History and Questionnaires
7.2.2.2 Physical Examination
7.2.3 Treatments
1. Selective Serotonin Reuptake Inhibitors (SSRIs)
2. Topical Anaesthetics
3. Psychotherapy
Other available treatments are as follows:
1. Phosphodiesterase type 5 inhibitors (PDE5i)
2. Topical Alprostadil cream (200/300 μg)
3. Tramadol
4. Alpha Blockers
7.3 Delayed Ejaculation (DE)
7.3.1 Aetiology
There are mainly three aetiological factors that are well-recognized in the context of DE [44].
1. Aging: degeneration of penile afferent nerves inhibits ejaculation.
2. Congenital: Mullerian duct cyst, Wolffian duct abnormalities, Prune Belly Syndrome, imperforate anus, and genetic abnormalities.
3. Anatomic causes: transurethral resection of the prostate, bladder neck incision, circumcision, and ejaculatory duct obstruction (can be congenital or acquired).
4. Neurogenic causes: diabetic autonomic neuropathy, multiple sclerosis, spinal cord injury, radical prostatectomy, proctocolectomy, bilateral sympathectomy, abdominal aortic aneurysmectomy, and para-aortic lymphadenectomy.
5. Infective/inflammatory causes: urethritis, genitourinary tuberculosis, schistosomiasis, prostatitis, and orchitis.
6. Endocrine causes: hypogonadism, hypothyroidism, and prolactin disorders.
7. Medications: antihypertensives, thiazide diuretics, alpha-adrenergic blockers, antipsychotics, antidepressants, alcohol, antiandrogens, ganglion blockers, and SSRIs. 8. Psychological: acute psychological distress, relationship distress, psychosexual skill deficit, disconnect between arousal and sexual situations masturbation style.
7.3.2 Diagnosis of DE
7.3.3 Treatment
1. Psychological support
2. Pharmacotherapy
3. Penile vibratory stimulation
7.4 Retrograde Ejaculation
7.4.1 Aetiology
7.4.2 Diagnosis of RE
7.4.3 Treatment
7.5 Anejaculation and Anorgasmia
7.5.1 Aetiology
7.5.2 Diagnosis
7.5.3 Treatment
