Sexually Transmitted Diseases - I. I. Mavrov 2005

Sexual Dysfunction in Men

Coitus interruptus (practiced by many men), prolonged sexual intercourse (coitus prolongatus), and sexual excesses play a significant role in The Development of functional sexual disorders.

Coitus interruptus refers to sexual intercourse in which the man, sensing the approach of ejaculation, withdraws his Penis from the Vagina to prevent conception. Such intercourse cannot be considered a disease in the clinical sense. However, interrupted coitus can cause physical and psychological disturbances. Under normal conditions, ejaculation should occur reflexively, without conscious effort; whereas during interrupted intercourse, the man constantly awaits the moment of ejaculation and orgasm with tense attention, striving to catch the onset of ejaculation while fearing to miss it. At the moment of orgasm, he uses a volitional effort to halt the reflex act, withdraws the penis, and ejaculation takes place outside the FEMALE REPRODUCTIVE Organs. Consequently, a man's sexual function may become impaired even when his sexual organs and prostatic secretions are completely normal, or it may lead to the development of pathological changes within them. In the genesis of sexual disorders associated with interrupted intercourse, not only local Changes in the male sexual organs play a role, but also A number of disturbances in the sphere of Higher Nervous Activity. This involves a sharp transition from sexual arousal to sudden inhibition, which disrupts the fundamental nervous processes of Excitation and Inhibition. In such cases, premature ejaculation, impaired erection, or prostate atony may occur.

Prolonged sexual intercourse refers to coitus that is deliberately delayed. The duration of a single act of intercourse is frequently very long, leading to the functional exhaustion of the spinal centers of erection and ejaculation, which in turn can cause impotence. As a result, neurotrophic changes appear in the male sexual organs due to insufficient and extremely slow venous drainage, causing congestive hyperemia in the Prostate Gland. This results in congestive prostatitis. For the same reason, the seminal colliculus may become edematous and hyperemic, and increased in size. The mucous membrane of the posterior urethral wall is likewise hyperemic and edematous.

Prolonging sexual intercourse by interrupting friction can lead to prostatic atony, which causes prostatorrhea, spermatorrhea, and—due to the atony of the musculature of the prostatic ejaculatory ducts—their incomplete closure. This causes one of the forms of impotence, and in some individuals, pathological pollutions and even Urinary Incontinence.

Such changes in the male sexual organs can result from prolonged sexual overexertion and extended erections without subsequent sexual intercourse, as well as from so-called vulgar sexual intercourse—penile friction inter labiae feminae. Similarly harmful is coitus incompletus, or incomplete sexual intercourse, where coitus is intentionally stopped short of ejaculation.

The harm caused by interrupted and prolonged sexual intercourse, as well as other abnormal sexual acts (vulgar, incomplete, etc.), lies in the fact that after numerous erections, neither ejaculation nor orgasm occurs, and after prolonged arousal, there is no resolution. This induces neurotrophic changes in the sexual organs, exhausts the spinal centers, and leads to the fading of cortical conditioned-reflex mechanisms. These changes can trigger sexual disorders.

Sexual excesses are extremely harmful in their consequences, especially for the young, physically unstrengthened Organism. Normally, a state of mild, quickly passing fatigue follows a regular sexual act. However, if sexual acts follow one another in rapid succession and each is prolonged, The Human Body has no time to recover, while frequent overstraining of The Nervous system causes its exhaustion and can become a cause of impotence.

Both in adolescence and adulthood, sexual excesses cause a dulling of the orgasm that should accompany normal sexual intercourse. They lead to a significant decline in sexual function and, by weakening the entire organism, hinder its normal development, eventually causing exhaustion of the spinal centers of erection and ejaculation, which precipitates sexual dysfunction. The absence of orgasm and the weakening of sexual function frequently become the cause of Sexual Perversions.

Oligospermia and necrospermia can be consequences of sexual excesses. Semen becomes thin and more transparent, and the count of spermatozoa and prostatic bodies within it decreases. Not only the quantity but also the quality of spermatozoa changes (their motility decreases and sometimes disappears altogether), and immature forms appear. In necrospermia, although semen is ejaculated in sufficient quantity, the spermatozoa are dead—completely immobile (even upon immediate examination of the semen after ejaculation).

Sexual excesses can cause anemia, Muscle weakness, loss of appetite, fatigue, malaise, headaches, palpitations, and pain in the genital region. They exert a particularly negative impact on the nervous and cardiovascular systems. Cases of myocardial infarction and fatal Cerebral Hemorrhage resulting from sexual excesses have been documented.

Thus, sexual excesses not only cause sexual disorders but can also be the ROOT cause of severe diseases in men. Therefore, a normal sex life and moderation in sexual contacts help preserve male sexual function over a long period.

Impotence is the inability of a man to achieve a full-fledged sexual act. It is a specific form of male sexual dysfunction, distinct from other disorders such as pathologies of libido, orgasm, sperm passage, or ejaculation. Impotence is caused by the inability to generate the pressure in the corpus cavernosum of the penis necessary for its insertion into the vagina, or to maintain this pressure until ejaculation occurs. Penile rigidity, which determines erectile capacity, is directly related to the ARTERIAL Blood PRESSURE inside the corpora cavernosa, which is approximately 90 mmHg. Ordinarily, this pressure is sufficient for the normal insertion of the penis into the vagina.

There are several classifications of impotence. Primary impotence is diagnosed when the patient has never experienced a period of normal sexual function, whereas secondary impotence refers to a previously functioning potency that has since been impaired. Recently, the most widely accepted Classification is based on the presumed pathophysiological mechanisms of impotence. Specifically, a distinction is made between impotence of primary psychological origin and organic impotence. Among the causes of organic impotence are mechanical trauma, vascular, neurological, and hormonal disorders, and combinations thereof.

According to traditional estimates of this condition, approximately 90% of impotence cases are psychologically driven. However, numerous recent studies place increasing emphasis on organic factors. Some papers report that organic pathology is detected in more than 50% of evaluated patients with impotence.

Psychogenic impotence. The primary foundation for deficient erections can lie in psychological factors. Men with erectile dysfunction frequently exhibit psychological alterations. The question sometimes arises as to when these alterations are the cause versus the consequence of impotence. Distinguishing between Primary and secondary psychological factors in erectile dysfunction requires a specialized evaluation.

The physical basis of impotence caused by primary psychological factors is inadequate stimulation of the corticosacral pathway. This can be triggered by many causes, notably the consequences of symptomatic hyperstimulation resulting from anxiety, depression, aggressiveness, or guilt during sexual stimulation. While psychological factors are present in such patients, in the majority of cases they do not serve as the primary etiological cause. Regardless of the presence of organic disease, feelings such as depression, aggressiveness, lowered self-esteem, and loss of self-respect are manifested in impotence. Patients with primary psychogenic impotence are typically relatively young (under 45 years of age) and report a sudden onset of the condition, usually linked to a quite specific incident. Occasionally, they experience "situational" impotence—the inability to engage in sexual intercourse under certain conditions.

Patients with impotence exhibit certain psychological disturbances, which is entirely understandable since self-esteem, self-respect, and self-awareness are frequently closely tied to the adequate execution of sexual function. Therefore, it is necessary to gather information regarding manifestations of anxiety, aggressiveness, depression, guilt, and inferiority feelings. However, it is sometimes difficult to establish whether these factors are the primary cause of impotence or its consequence. Psychogenic impotence is characterized by a polymorphic clinical picture, fluctuations in the severity of sexual dysfunction, and success in one specific situation alongside persistent inadequacy under other conditions. Concurrently, patients exhibit a decrease in sexual drive and a predominance of inhibitory factors despite a preserved sex drive.

Patients with a diminished sexual drive report sexual weakness, but detailed questioning reveals that both erection and ejaculation are preserved, yet either the desire for sexual intimacy is absent or this desire is expressed inadequately and vaguely, being fulfilled out of a sense of duty rather than need. Some patients fail to experience an erection even under certain favorable circumstances. Others derive no satisfaction despite the full physiological realization of the sexual act.

When sexual drive is preserved, patients exhibit diverse symptoms: inadequate erection, sometimes its complete absence, overly rapid ejaculation, or conversely, aspermatism. The most characteristic sign is considered to be the disappearance of an adequate erection at the most critical moment, right before THE START OF intercourse, whereas the preparatory phase proceeded normally. Spontaneous erections in the morning or during erotic fantasies, coupled with their disappearance in a real intimacy situation, are also characteristic.

Patients are encountered whose decreased sexual drive stems from many years of sexual abstinence, negative or distracting influences, preoccupation with work, a negative attitude toward their wife due to her frigidity, chronic overfatigue, prolonged anxiety, or emotional depression. An inadvertent offensive word can cause sexual dysfunction; for example, a wife's reproaches regarding a man's sexual impairments become a pathological stimulus that severely exacerbates the existing condition and induces deep erectile inhibition.

Consequently, any negative emotion that even indirectly disrupts the integrity of a man's sexual urge can acquire a pathogenic character and firmly entrench the resulting disorder. Failures during casual sexual encounters provoke particularly strong distress. Even more acute is the distress experienced during a crisis situation on the wedding night, when an unexpected failure jeopardizes future marital relations.

The sudden loss of an adequate erection exerts a sharply traumatic impact, leading to the impossibility of intimacy. An unexpectedly experienced premature ejaculation prior to intercourse holds exceptional pathogenic significance, especially if this occurs before the first intimate encounter. The pathogenic impact of this experience can be so strong that a man remains convinced of his inadequacy and hesitates to initiate a sexual life for a long time (sometimes several years).

Organic impotence is the inability of a patient to achieve and maintain an erection, unrelated to psychogenic factors. Vascular pathology is the most frequent cause. The internal iliac-pudendal Arterial System, which supplies blood to the penis, comprises the internal pudendal artery, the penile Arteries, and the Arteries of the corpora cavernosa. This system possesses a unique capacity to drastically increase BLOOD FLOW IN response to sexual stimulation of the pelvic visceral (autonomic) nerves. Normally, blood flow is 10 mL/min at rest and approximately 60 mL/min during stimulation (P. Metz, E. Wagner, 1981). Such a rapid increase in blood flow, alongside its neurogenic redistribution into the corpora cavernosa, triggers an erection.

Insufficient blood pressure in the small Vessels of the arterial bed during sexual stimulation results in inadequate Blood supply to the corpora cavernosa and an incomplete erection. This apparently explains the close association between impotence and Aging. The degree of arterial bed impairment can vary. For instance, the complete absence of erection may indicate severe vascular pathology, whereas relatively good resting erections that disappear during copulatory friction may manifest a less severe vascular disease.

If blood inflow into the iliac arteries is restricted and occlusions are present in the internal pudendal artery, blood flow is redistributed into the lower-resistance vessels of the skeletal Muscles. Such vessels are located in the gluteal muscles, supplied by the superior and inferior gluteal arteries, which branch off from the iliac and internal pudendal arteries. In clinical practice, this stress-induced blood flow redistribution is termed the pelvic "steal" syndrome. It may manifest as the disappearance of erections during active coital friction.

Vascular impotence is most commonly observed in patients with a history of arterial Hypertension, Diabetes Mellitus, peripheral vascular disease, coronary artery disease, and cerebrovascular insufficiency. Smoking plays a significant role in the development of vascular impotence. A distinct patient group comprises those with vascular impotence resulting from blunt perineal trauma or pelvic Radiation therapy.

The decline of erectile function in vascular impotence may be gradual, manifesting as less frequent sexual intercourse, normal or premature ejaculation, inadequate erections in response to sexual stimulation, and the inability to maintain an erection until ejaculation. The Use of antihypertensive medications by these patients further contributes to the impairment of erectile function.

Evaluation of such patients involves assessing the state of The Vascular System. This is done by palpating the pulse of the dorsal artery of the penis at the level of the suspensory ligament and grading it on a four-point scale (from 0 to 3). The pulse in other arteries, such as the femoral artery, provides insight into the status of the proximal aortoiliac segment or stenosis of the external iliac artery. However, a distinct pulse in the femoral artery does not rule out distal small-vessel disease within the ilio-pudendal arterial bed. Other signs of peripheral vascular disease, including lower extremity muscle atrophy, Skin pallor, and Hair loss on the lower limbs, may indicate systemic vascular disease.

When evaluating impotence, the ilio-pudendal arterial bed must be examined. The adequacy of pelvic blood flow is typically assessed non-invasively using penile Doppler Ultrasonography. For this Procedure, a standard 9.5 MHz Doppler probe is placed over each of the cavernous body arteries. A 2.5-cm-wide cuff is wrapped around the Base of the penis, and the occlusive systolic pressure in its arteries is measured. This value is then compared with the systemic occlusive pressure in the brachial artery to establish the penile-brachial index (PBI). At rest, the PBI helps detect blood pressure gradients caused by stenosis of the ilio-pudendal arterial bed. Since resting PBI has limited sensitivity, it is also measured dynamically or during physical exertion. If a pelvic "steal" syndrome is suspected, the patient performs gluteal muscle exercise for 3–5 minutes. A significant drop in PBI during exercise confirms the Diagnosis of steal syndrome, which is explained by The phenomenon of blood flow redistribution in the pelvic arteries during exertion: instead of entering the high-resistance ilio-pudendal arterial bed, blood is diverted to the gluteal arteries, which offer lower vascular resistance. Detecting this redistribution phenomenon during gluteal muscle exercise helps identify patients with vascular impotence who might otherwise have normal resting PBI values.

The redistribution phenomenon is also confirmed by measuring urethral Temperature during physical exertion. Urethral temperature closely mirrors the temperature of the cavernous bodies. A drop in penile temperature during physical exertion indicates a redistribution of blood flow within the pelvic arteries.

Other non-invasive Methods for determining pelvic blood flow include plethysmography and radioisotope studies. Selective internal pudendal arteriography is generally performed only in patients who have shown abnormal findings on non-invasive tests and who are willing to undergo invasive Procedures (such as balloon angioplasty, macro- or microvascular reconstruction). Internal pudendal arteriography should not be used solely for diagnostic purposes unless vascular revascularization is planned.

A fairly common form of organic impotence is neurogenic impotence. Normal sexual function relies on a healthy nervous system; therefore, any disturbances to it (such as neurosis, neurasthenia, Spinal Cord lesions, and pelvic parasympathetic nervous system disorders) can cause impotence.

Neurogenic factors can impair both the initiation and the maintenance of erections. Erections are mediated by three main neurological mechanisms. The first, the efferent pathway, involves the parasympathetic pelvic splanchnic nerves. It originates in the sacral segments (S₂, S₃, and S₄) of the spinal cord and terminates in the Blood Vessels of the cavernous bodies. Presumably, there are preganglionic nerve fibers utilizing acetylcholine as a neurotransmitter, as well as postganglionic fibers whose neurotransmitter remains unknown. Research in this field is ongoing, and it is entirely possible that vasoactive intestinal Polypeptides play a significant role in regulating blood flow redistribution within the cavernous bodies under the Influence of the pelvic splanchnic nerves. Pathology affecting these nerves (such as surgical trauma or diabetic autonomic neuropathy), as well as Disorders of the cauda equina or sacral spinal cord, can lead to impaired blood flow redistribution and inadequate pressure within the cavernous bodies.

The second efferent pathway is represented by the somatic pudendal nerve. It originates from cutaneous receptors in the genitalia, extends to the sacral segments (S₂, S₃, and S₄), ascends via spinal cord pathways—forming synapses in the area of the cortico-medullary junction and thalamus—and terminates in the contralateral primary sensory cortical area. Structure/19.html">The Importance of this pathway for normal sexual system function has been demonstrated in experimental and clinical studies (W. De Groat, A. Booth, 1980). Pathology in this neural mechanism can cause an inability to maintain an erection during coitus.

The third, cortico-sacral efferent mechanism comprises numerous Neural Pathways. Experimental studies in this area have identified the most critical brain regions controlling erection, notably the anteromedial Hypothalamus, paraventricular Nucleus, medial Forebrain bundle, gyrus rectus, septum pellucidum, mammillothalamic tracts, cingulate gyrus, and hippocampus. Cerebral impulses from these and other pathways travel through the substantia nigra of the Midbrain to the ventrolateral Regions of the Pons (M. Siroky, R. Krane, 1979). Descending tracts then Relay this information to the parasympathetic nuclei of the sacral spinal cord. Central control of erection is exercised through this pathway. Pathology of the cortico-sacral efferent pathway (such as multiple sclerosis, syringomyelia, transverse myelitis, or HEAD trauma) can adversely affect the conductivity of the parasympathetic pelvic splanchnic nerves and lead to erectile dysfunction.

Patients complaining of erectile dysfunction should routinely undergo a neurological examination, especially if they have a history of neurological disorders or underlying nervous system pathology.

The neurological examination should focus primarily on the perineal region and lower extremities. It is essential to assess cutaneous sensitivity of the external genitalia and lower limbs to light Touch and pinprick. Deep tendon Reflexes are evaluated, including the quadriceps reflex (L₃, L₄) and the Achilles reflex (L₅, S₁, S₂). Bulbocavernosus reflexes are assessed by palpating the glans penis. Muscle contraction is detected by fingers placed over the bulbocavernosus muscle or the external anal sphincter. Normally, most men exhibit cavernous reflexes, the reflex arc of which is mediated through the sacral segments S₂, S₃, and S₄.

The vibratory sensory threshold of the penis is also determined. This procedure is performed using a biothesiometer; it is inexpensive, completely painless, and provides quantitative and reproducible results. Abnormalities in vibratory sensitivity serve as an early sign of peripheral neuropathy. Sensors are placed on the right and left sides of the glans and shaft of the penis. The patient is asked to indicate when they perceive the vibration while the vibration amplitude is gradually increased. The test is repeated until reproducible results are obtained. Because this test involves minimal nerve stimulation, it is considered a reliable indicator of peripheral sensory neuropathy within the pudendal nerve system.

Other neurological investigative methods include perineal electromyography, sacral nerve latency testing, and the recording of cortical brain potentials in response to external genital stimulation, among others. Correlating objective neurological findings with the results of other erectile function tests allows for a more precise diagnosis of neurogenic impotence.

Depending on the Etiology of the neurological lesion, the onset of the condition may be gradual or sudden. Erections may disappear entirely or become incomplete, characterized by insufficient penile rigidity. Potency can be affected by neurological disorders associated with alcoholism, diabetes mellitus, status post radical pelvic surgery, spinal cord infections, tumors or trauma, intervertebral disc degeneration, as well as Brain Tumors, cerebral trauma, or cerebral insufficiency. Frequently, impotence is caused by a combination of neurological and vascular factors, such as in patients with diabetes mellitus.

Endocrine-origin impotence. This type of pathology, caused directly by endocrine disorders, is relatively uncommon and may be associated with hypogonadism, hyperprolactinemia, hyperthyroidism, and elevated estrogen levels. Abnormalities of the hypothalamic-pituitary-gonadal axis or other endocrine systems can impact The ability to achieve and maintain an erection. The pathophysiological mechanism of this type of impotence remains poorly understood. Currently, it is unclear how endocrine disorders affect blood flow into the cavernous bodies or local microvascular redistribution. On the other hand, the central mechanism controlling libido is unquestionably influenced by endocrine factors.

Certain conditions, such as Liver cirrhosis, are accompanied by altered estrogen METABOLISM; therefore, a patient history regarding alcohol consumption and previous hepatitis is essential. Therapeutic administration of estrogens, for instance in the Treatment of prostate Cancer, can reduce libido. Basophilic Adenoma of the anterior Pituitary Gland leads to generalized feminization, intersexual appearance, and impotence in men. Adrenal cortical disorders are also frequently associated with impotence and decreased sexual desire.

Endocrine System evaluation is based on the assessment of secondary sex characteristics: body and facial hair distribution, Muscle Development, size and consistency of the prostate gland and Testes, as well as the level of androgenic stimulation. The presence or absence of gynecomastia indicates altered estrogenic stimulation.

The minimal endocrinological workup for a patient with impotence should include measuring plasma concentrations of testosterone, luteinizing hormone, and prolactin. This evaluation is indicated for all impotent patients, particularly those reporting decreased libido. In some cases, a more comprehensive assessment of potential endocrine abnormalities is performed, including the evaluation of alternative testosterone metabolic pathways (levels of estrone, testosterone metabolites such as dihydrotestosterone, estradiol, and the unbound fraction of testosterone, i.e., free testosterone). An in-depth investigation includes determining the levels of all gonadotropin fractions, testosterone, and estradiol; 24-hour urine collection for 17-ketosteroids; sella turcica polytomography; computed tomography and visual field testing; human chorionic gonadotropin stimulation testing; and assessing gonadotropin release in response to luteinizing hormone-releasing hormone (LHRH).

The classic manifestation of endocrine-induced impotence is a decrease in libido. Subtle clinical signs, such as underdevelopment of the testes and sparse body hair, may point toward hypogonadism. Hyperprolactinemia may be accompanied by depression and visual impairment. Sweating and fine finger tremors can be symptoms of hyperthyroidism. A low testosterone level does not necessarily indicate an endocrine etiology for impotence. Clinical observations confirm that normal erections are possible even in patients with testosterone levels significantly below normal, as well as in castrated individuals.

Impotence due to mechanical obstructions. The primary symptoms include difficulty in performing sexual intercourse due to abnormal penile positioning, penile curvature, painful erections (Peyronie's Disease), partial or total penectomy, and congenital penile defects such as severe epispadias and micropenis.

Causes of this form of impotence may include a large scrotal hernia, a short frenulum causing penile curvature during erection, scrotal lymphedema (elephantiasis), penile deviation following traumatic rupture of the cavernous bodies, and occasionally extreme hypersensitivity of the glans (especially post-trauma).

Medication-induced impotence. It is well established that many drugs, primarily antihypertensive agents, can cause impotence. The exact mechanism of drug-induced impotence is poorly understood, but it likely involves both central and peripheral effects. Potential peripheral effects include altered perfusion, direct blockade of neurotransmitter action during pelvic nerve stimulation, and a generalized reduction in systemic blood pressure. Even with mild vascular stenosis, adequate blood flow into the cavernous bodies becomes possible only under elevated systemic pressure. Consequently, some patients experience normal erections only after discontinuing antihypertensive medications, whereas under controlled hypertension, erections remain suboptimal. However, a more severe vascular occlusion is more frequently observed, where erections do not fully recover even after stopping antihypertensive therapy. This may explain the Adverse effects of hydrochlorothiazide on sexual function. Impotence can also be triggered by Diuretics, tranquilizers, sympatholytics, and antidepressants.

In some cases, impotence develops as a result of intoxication caused by leaded gasoline, lead, various acids, nitro compounds, and other occupational hazards (such as Vibration disease), as well as following prolonged and severe infectious illnesses.

Impotence caused by Inflammatory Diseases of the reproductive organs. Inflammatory processes in the genital organs caused by Sexually Transmitted Infections (such as chlamydia, mycoplasma, Gonorrhea, and Trichomoniasis) are frequently a cause of impotence. The Pathogenesis of these disorders is twofold: impotence may develop as a direct consequence of structural damage to the reproductive organs (prostate gland, seminal colliculus, Seminal Vesicles), or it may be psychogenic in origin. In impotence caused by these conditions, along with damage to the receptor apparatus, impairments in other links of neural regulation of sexual function are observed—specifically, spinal sexual centers become involved in the pathological process. Patients frequently exhibit various neurological disorders.

The chronic course of inflammatory processes in the reproductive organs, frequent relapses, fear of complications that may lead to sexual dysfunction, and patients' excessive fixation on their condition create a constant and prolonged traumatic psychological situation. Often, a patient's attempt to have intercourse ends in failure due to the lack of an adequate erection at the crucial moment. As a result, the clinical course of impotence worsens.

The clinical picture of impotence caused by inflammatory lesions of the reproductive organs is characterized by a progressive decline in potency with weakened erections while sexual desire remains preserved. However, in some cases, patients also experience a decrease in libido. Typical symptoms include weakness, Sleep disturbances, reduced working capacity, and depression, which are triggered by sexual dysfunction and can themselves become causes of functional disorders.

Diagnosing impotence presents certain challenges given the complex pathophysiological mechanism of this condition and the fact that impotence is not merely a psychological issue. Proper attention must be paid to diagnostic strategies for identifying the pathophysiological foundations of impotence, thereby ensuring the Selection of effective treatment methods.

Clinical examination frequently reveals symptoms that support the pathophysiological hypothesis of impotence derived from the patient's history. A carefully taken history—both general and sexual—ensures a proper Assessment of the pathophysiological causes of impotence. The sexual history includes questions related to sexual dysfunction. First and foremost, the physician should clarify what the patient means by impotence (as it is frequently confused with decreased libido or ejaculation disorders); establish the onset time of the sexual disorder and The Nature of its development (whether it began suddenly or gradually); determine the frequency of sexual intercourse currently and prior to the illness; assess the ability to ejaculate, whether erections are insufficient, whether premature ejaculation occurs, or both simultaneously; and ascertain whether weakened erections and premature ejaculation are occasional occurrences. It is very important to determine whether the desire for sexual intimacy exists, and what the quality of the erection is during sexual stimulation with a regular partner and other partners.

The sexual history should be sufficiently detailed so that, taking the aforementioned data into account, the type of impotence can be determined. In patients with impotence primarily caused by psychological factors, a sudden change in potency over several days or weeks is possible, with erection quality depending heavily on the situation. This is more commonly observed in young men, bachelors, individuals who do not lead a regular sex life, when attempting intercourse in inappropriate environments, or during a first-ever sexual experience. Such patients typically complain of libido and ejaculation disorders.

Ejaculation disorders, particularly premature ejaculation, frequently lead to partner dissatisfaction, rob the patient of self-confidence, induce a fear of failure, and serve as a source of anxiety.

Patients with organic impotence (usually of vascular origin) note a gradual fading over the years of their ability to achieve erections—declining from several acts of intercourse per week to sporadic intercourse over the course of a month. Libido is usually preserved, ejaculations occur normally or slightly prematurely, and erections are inadequate regardless of sexual stimulation.

However, confirming the pathophysiological hypothesis requires an objective evaluation of erectile function. For instance, patients whose impotence is rooted in psychological factors may deny having morning erections and report a gradual (rather than sudden) change in erectile capacity. Conversely, if the condition is organic in origin, morning erections may be entirely normal, and changes in erectile function are more likely to occur suddenly—especially if they coincide in time with radical pelvic surgeries, trauma, exposure to chemical agents or other hazards (short and ultra-short waves, leaded gasoline, high temperatures, etc.). At the same time, patients with organic impotence may also exhibit disorders that completely mask the organic etiology of the disease, while objective symptoms are frequently absent upon examination.

During the general history-taking, the physician investigates what infectious or other illnesses the patient has suffered from; whether, In addition to these illnesses, the patient has experienced severe psycho-emotional distress or occupational and domestic troubles; whether they smoke (and how many cigarettes per day); and when they started consuming alcohol (frequency and quantity), among other factors.

When examining patients with impotence, it is crucial to identify risk factors (cardiovascular diseases and family history thereof, hypercholesterolemia, arterial hypertension, diabetes mellitus, as well as past neurological diseases, strokes, and spinal surgeries), determine whether limb weakness, urinary or defecation disorders have been observed, and detect prior illnesses or endocrine disorders. It is essential to know precisely which medications the patient has been taking, particularly whether they have used hypotensive agents.

The diagnostic evaluation of a patient with impotence is not limited to taking a medical history and conducting a physical examination. A series of additional studies is performed to clarify certain physiological mechanisms of erection (including the assessment of nocturnal erections), determine the state of the vascular and endocrine systems, evaluate neurological status and mental health, and examine the patient's relationship with their spouse and living conditions.

A correct Cytology/practical/136.html">Differential diagnosis OF impotence largely determines the success of treatment, as it facilitates the selection of rational therapy, which may include psychotherapy, hormone replacement therapy, pharmacotherapy, prosthetic surgery, or reconstructive vascular and microvascular interventions.

Treatment and Prevention. Depending on the form of impotence and the manifestations of the disease, various treatment methods are applied. For instance, in cases of impotence primarily caused by psychological factors, psychotherapy is usually the mainstay; for organic forms, mechanical damage, vascular disorders, or neurological deficits are corrected; while endocrine-related impotence is managed with hormone replacement therapy.

The treatment of impotence caused by intoxications, severe infectious diseases, or inflammatory processes in the reproductive organs must be individualized and comprehensive, involving various pharmacological agents and physiotherapy. Taking into account any neurological disorders the patient may have, it is advisable to combine psychotherapy with the Treatment of the underlying pathological process.

Pharmacological treatment should take into account the General mechanism of action—such as Central nervous system sedatives or stimulants, general tonics and biogenic stimulants, vitamin therapy, and so forth. At the same time, it should be kept in mind that many medications (primarily antihypertensive drugs) can induce impotence.

Since The problem of impotence is relevant to millions of men, a systematic, comprehensive approach to its resolution is widely practiced today. When diagnostic strategies are tailored to the individual CHARACTERISTICS OF THE patient, treatment becomes maximally effective. In some cases, thanks to The Emergence of new treatment methods—particularly microsurgical vascular reconstruction—impotence can be resolved without resorting to prosthetics.

Ejaculation disorders. These include premature ejaculation and delayed ejaculation. They are frequently observed while the ability to achieve normal erections remains intact. In some cases, ejaculation occurs even before the penis enters the vagina. Premature ejaculation can be very rapid, sometimes instantaneous.

In a healthy man, ejaculation occurs on average after 30–50 friction movements, but these figures can vary and, depending on individual characteristics, fluctuate within a wide range. Ejaculation typically occurs 2–6 minutes after the onset of intercourse. Premature ejaculation is rarely caused by organic factors.

It should be kept in mind that after prolonged sexual abstinence or extended sexual arousal preceding intercourse, the first—and sometimes subsequent—acts end in rapid ejaculation. One can determine whether a patient suffers from premature ejaculation by comparing the current duration of intercourse with that in the past.

In cases of delayed ejaculation, emission does not occur during intercourse despite the fact that the man's body produces seminal fluid and spermatozoa. This rare form of sexual disorder can be temporary or permanent and is most commonly caused by psychogenic factors. It arises as a result of decreased or completely absent excitability of the ejaculation center while the function of the erection center remains normal (spinal aspermatism). Sexual desire, erection, and the duration of intercourse are normal in such patients. However, despite the absence of organic barriers to the release of semen, ejaculation during sexual intercourse does not occur, and orgasm is absent (anorgasmia).

The causes that damage spinal sexual centers are diverse. They include spinal cord diseases, lumbar spine trauma, sexual excesses, sexual arousal without subsequent intercourse, alcohol abuse, treatment with alpha-blockers, chronic infectious diseases (tuberculosis, Syphilis), and occasionally retroperitoneal surgery.

In some cases, aspermatism develops due to the obliteration of the ejaculatory ducts, urethral strictures, loss of tone in the internal urinary sphincter, and purely mechanical damage to the vas deferens (mechanical aspermatism). Excitation of the ejaculation center may also be insufficient in the presence of scarring on the glans penis or prepuce.

Ejaculation disorders cause a profound sense of dissatisfaction during intimacy for both men and women, frequently trigger conflicts in marital life, and drive individuals to seek extramarital sexual contacts.

The treatment of ejaculation disorders consists of eliminating their underlying causes. During therapy, abstinence from sexual intercourse is usually recommended. When addressing a combined correction of both cortical and spinal sexual mechanisms, psychotherapy is prescribed. Various methodologies, options, and combinations are utilized. Hypnotherapy is also integrated into the comprehensive psychotherapeutic approach. Its outcomes depend primarily on the effectiveness of treating the primary disease.

When seminal duct patency is impaired due to inflammatory diseases or Congenital Malformations, Surgical treatment is recommended. The anatomical Location OF THE obliteration site is critical to the surgical outcome. If the blockage is localized in the scrotal or inguinal segment, treatment is generally effective. When obliteration occurs in the tail of the Epididymis while the patency of the vas deferens remains intact, an anastomosis of the vas deferens to the proximal portion of the epididymis or its head is performed; if the obliteration is located in the head of the epididymis, an anastomosis of the vas deferens to the Testis is carried out.

Satyriasis is a pathological increase in sexual drive in men, characterized by a persistent sense of dissatisfaction and an insatiable urge for sexual intercourse. It is identified by the following signs:

a) in terms of the intensity of sexual activity, when a man, consumed by desire, possesses a woman with extreme intensity. Restraint is difficult for him. His ability to subordinate his emotions to reason is limited. Driven by his sexual drive, he may behave immodestly toward his partner, people around him, and even himself, yet after satisfying his sexual needs, he often regrets his behavior;

b) in terms of the frequency of the urge, when a man, having barely achieved satisfaction, is once again obsessed with sexual hunger, capable of engaging in multiple acts of intercourse daily, and seeks release outside of marriage at every opportunity;

c) in terms of the rapidity with which sexual arousal develops. Upon encountering appropriate stimuli, a man immediately feels the desire for sexual intimacy (even with the slightest physical contact, such as while dancing, upon seeing an attractive woman, during fantasizing, etc.) and cannot wait to satisfy his sexual need;

d) in terms of the emergence of intense sexual arousal triggered by A wide variety of stimuli that provoke a desire for sexual intimacy—such as the sight of almost any woman, specific PARTS OF THE female body, photographs, erotic conversations, certain types of music, scents, and several other factors.

Increased sexual drive as a syndrome can be observed in various pathological conditions (encephalitis, traumatic or vascular brain injuries, brain tumors, adrenal hyperfunction, psychoses, etc.), as well as during periods of stress or following intense physical exertion.

Satyriasis is relatively rare in healthy men. However, in practice, dermatovenerologists occasionally encounter patients who report an exceptionally intense, insatiable drive leading to an extraordinarily high number of sexual contacts and promiscuity regarding sexual partners.

Excessive increases in sexual drive in men require a thoughtful approach from the physician. It is essential to consider that complaining of heightened sexual drive is very difficult for patients due to the prevailing negative societal stigma toward such individuals.

Individuals with an elevated sexual drive primarily require the correction of their moral and ethical attitudes. Such patients are advised to resolutely and meticulously eliminate stimuli that provoke sexual arousal and to avoid situations that stimulate sexual urges. Patients are encouraged to engage in physical labor, physical training, and sports; the use of sedatives, including hypnotics, is indicated to alleviate the intensity of sexual urges.