Sexual relations are not just biological function which is essential for provision of future generation, but also an important part of life, source of joy and love. Therefore, it is not coincidence that sexual disorders are considered to be a serious medical problem. Structure of sexual disorders has erectile dysfunction on its top, since in accordance with the latest data; it is widely-spread all around the globe. More than 30 per cent of men at the age of 18-59 years have disorders of erectile dysfunction of different severity level. Prolongation of longevity led to increase of a number of men suffering from impairments of sexual function.

In structure of sexual disorders, diabetes comprises more than 40 per cent of cases, i.e. practically every second patient suffering from ED is a diabetic. Erectile dysfunction is a typical complication of diabetes which is along with other well-studied complications (diabetic micro-and macrovascular complication, diabetic polyneuropathy, diabetic retinopathy, etc.) leads to considerable impairment of patient’s quality of life.

Even the thought of possibility of sexual function impairment in any man takes adverse impact in psychic condition and may become a cause of depression which in turn may result in ED development. It goes without saying that active exposure of ED requires understanding of this problem and knowledge of its solutions. Not only urologist, andrologist, sexologist, diabetologist and endocrinologist, but also general practitioner must understand biological and psychological foundations of sexuality and be able to interview such patient.

Erectile Dysfunction: Definition and Classification of Neurogenic Disorder

Erectile dysfunction is incapacity to achieve and (or) preserve erection for sexual intercourse in the half and bigger number of cases. While diagnosing ED, it is important to determine the cause of impairments. Based on these data, a specialist can conduct a differential diagnostics of various forms of erectile dysfunction and select corresponding pathogenic therapy. It is extremely important to distinguish ED forms, since they differ not only in treatment approaches, but also forecast regarding restoration of sexual function.

Psychogenic character of erectile dysfunction may be diagnosed in patients on the setting of absence of somatic pathology. Any sexual frustration may be accompanied by fear of failure. It may be resulted from frequent focus of attention on erection and as a consequence – decrease of psychogenic component of its occurrence. Long-term progression of erectile dysfunction leads to the fact that sexual life recedes into the background and the so-called “syndrome of desactualization” appears which means decrease of impact of psychogenic component on erectile function.

Organic character of erectile dysfunction may be a sign of presence of a particular somatic disorder (for instance, arterial hypertension, obesity, hypogenitalism, etc.). Exposure of certain risk factors leading to development of organic ED also helps in conduction of differential diagnostics. Detection of impairments of sexual function should be taken very seriously, since sexual function disorder (especially in patients with diabetes) is the first sign of neuropathy. Early stages of neuropathy may be only accompanied by feeling of cold in the area of balanus which is called a syndrome of cold balanus.

Organic ED induced by neuropathy may be exposed by a simple test: determination of temperature sensitivity of penis.

Neurotransmitters mediating erectile response are not enough studied, but include acetylcholine and other non-adrenergic, non- cholinoceptive messengers. Final neurotransmitter is active vasodilator – nitrogen oxide which penetrates inside smooth muscle cells of cavernous bodies, i.e. acts intracellularly causing boost of cyclic guanosine monophosphate level. cGMP launches complicated chain of reactions which in the end leads to relaxation of smooth muscle cells and occurrence of erectile response. Cyclic guanosine monophosphate gets split further under the influence of phosphodiesterase type 5 which is specific for cavernous bodies. Thus, erection decline occurs.

The main sources of nitrogen oxide secretion (key neurotransmitter of erection) are cavernous nerves; therefore, neuropathy plays an important (even dominant) role in ED development, since occurrence of normal erection is not possible in case of normal condition of vessels and normal endocrine status. It should be mentioned that diabetes is not a sole cause of neurogenic ED development.

Neurogenic ED is divided as follows:

• diabetic neurogenic ED;
• traumatic neurogenic ED (very often after operations on pelvic organs and penis);
• toxic neurogenic ED (on the setting of alcohol addiction, long-term intake of medicinal products);
• age-related neurogenic ED (due to decrease of testosterone secretion).

Hyperglycemia (learn more about this disease) is an essential factor of neuropathy progression, since provision of glucose in neurons, neurilemma cells and their appendages doesn’t depend on insulin. Clinically, this is confirmed by data regarding decrease of neuropathy decrease by 40-60 percent in case of optimal glucose content control in blood.

Therapy of Neurogenic Erectile Dysfunction

Nowadays, selection of remedies for ED treatment is rather large which allows practically each patient suffering from erectile disorder to select effective therapy with medicamentous or surgical methods. Thus, it should be borne in mind that there are no incurable forms of ED. Nevertheless, a number of patients resistant to classical therapy implying the intake of PDE5 inhibitors are rather big. Considerable contribution to the therapy with PDE5 inhibitors is made by under-diagnosis of neurogenic ED.

Over the last years, pathogenic therapy of diabetic neuropathy is treated with alpha-lipoic (thioctic) acid with pronounced antioxidant effect. This acid restores impairment of relaxation of unstriated muscles in cavernous bodies caused by neuropathy. Alpha-lipoic acid is a physiological antioxidant taking impact on excessive production of free radicals which occurred due to oxidizing stress. This acid takes pronounced neuroprotective, endoprotective and hepatoprotective action causing decrease of hepatosis with lipotropic action.

It is important that alpha-lipoic acid is active substance with critical bioaccessibility. In some cases, this leads to the fact that peroral therapy with tis acid doesn’t cause the achievement of effective level and patient’s response is absent.

All in all, alpha-lipoic acid is the only pathogenic remedy for therapy of neurogenic ED. Its mechanism of action provides:

• increase of endoneurial blood flow;
• decrease of endoneural oxidizing stress due to restoration of endoneural antioxidant system;
• enhancement of endoneural absorption of glucose leading to energy storage in nerve;
• increase of initially reduced level of myoinositol in diabetic nerve;
• neurotrophic support;
• improvement of endothelial dysfunction.