Obstetrics and Gynecology - A. M. Gromova 2000

Menstrual Disorders
Forms of Menstrual Cycle Disorders
Neuroendocrine Syndromes

Climacteric Syndrome

The climacteric period is a transitional stage in a woman's life between the reproductive years and the permanent cessation of ovarian hormonal function. In most women, this transition occurs between the ages of 45 and 50 as a physiological process of general age-related bodily involution, proceeding without marked pathological signs. For some women, however, the climacteric period takes a pathological course, known as climacteric syndrome (CS). It manifests through endocrine, neuropsychiatric, autonomic-vascular disorders, and metabolic changes, affecting 25–30% of women of climacteric age. Disturbances in the Central Nervous system play a major role in the Pathogenesis of climacteric syndrome.

Class="center">Climacteric Disorders

The wide range of symptoms characteristic of climacteric syndrome can be divided into three main groups:

- neurovegetative;

- metabolic-endocrine;

- psychoemotional.

The severity of CS is assessed by the frequency of hot flashes (Vikhlyayeva E.M., 1970): mild CS involves up to 10 hot flashes per day with preserved general well-being and working capacity; moderate CS involves 10–20 hot flashes per day accompanied by other prominent symptoms such as headache, precordial pain, deterioration of general well-being, and reduced work capacity; severe CS is characterized by frequent hot flashes (more than 20 daily) and sometimes symptoms leading to significant or nearly complete loss of working capacity.

Treatment for patients with climacteric syndrome is managed collaboratively by a general practitioner, neurologist, and gynecologist, and should be administered in a phased approach:

Stage I – pharmacotherapy using measures that enhance the body's adaptive capacities, physiotherapy, and herbal medicine;

Stage II – non-hormonal pharmacotherapy;

Stage III – hormonal treatment for CS.

Patients require a well-regulated hygienic regimen with adequate physical activity, A balanced diet, vitamin therapy, remedial gymnastics, and physiotherapeutic Procedures (such as Davidov’s anodic galvanization of the Brain, galvanic collar with novocaine, bromine, or magnesium sulfate, and transnasal novocaine Electrophoresis). Acupuncture, hypnosis, climatotherapy, and balneotherapy are also effective.

Non-hormonal pharmacotherapy aims to normalize the functional state of the central Autonomic nervous system. Sedatives, tranquilizers, neuroleptics (such as etaprazine, triftazine, phenibut), and antihistamines (Tavegyl, Suprastin) are prescribed. If neither the sympathetic nor parasympathetic nervous system is clearly dominant, medications with adreno- and cholinolytic action (Belloid or Bellataminal) are used. Daily supplementation with Vitamins A, B₁, B₆, E, and ATP is prescribed. Vitamin D, ossin (sodium fluoride), and calcium supplements are used for the Prevention and treatment of osteoporosis. Homeopathic remedies such as Remens and Klimaktoplan may also be utilized.

If prior treatment stages fail to yield results, and taking into account the frequent presence of hypoplastic processes, hormone therapy is introduced using combined estrogen-progestogen preparations (Climonorm, Progynova, Klimen, Divina), conjugated estrogens (Premarin), or pure progestogens (progesterone, Primolut-Nor). For emerging menopausal symptoms, Livial (tibolone), a single-component drug with estrogenic, progestogenic, and androgenic activity, is prescribed at 1 tablet nightly for 3–6 months. In severe cases of CS accompanied by dystrophic changes in The Cardiovascular system, osteoporosis, and impaired urogenital function, combined estrogen-androgen preparations (Gynodian Depot, Ambosex) are prescribed for 1–1.5 years. For vaginal dryness and pruritus of the external genitalia, estrogen-containing vaginal suppositories (Ortho-Gynest, Ovestin) are used. Drug administration requires ongoing medical supervision. In the event of uterine bleeding, Diagnostic curettage of the uterine cavity is indicated.

Postcastration Syndrome

This syndrome is characterized by a complex of disorders that develop following surgical removal of the Ovaries or Radiation therapy due to the cessation of ovarian function and the consequent activation of the hypothalamic-pituitary system, resulting in excessive synthesis of gonadotropins and other Pituitary Hormones (somatotropin, ACTH, thyrotropin). The clinical picture resembles that of climacteric syndrome, presenting with various vasomotor, neuropsychiatric, and metabolic disorders. The severity of the condition depends on the patient's age (being more severe in younger patients) and her baseline health status prior to surgery. Postcastration syndrome typically manifests a month post-surgery and lasts for 2 to 5 years.

Treatment for a patient with postcastration syndrome should be comprehensive, aimed at normalizing the regulatory function of the central nervous system, enhancing the body's adaptive capacities, and stabilizing hormone secretion. It includes sedatives, tranquilizers, general tonics, vitamins (B₁, B₆, C), and hormone replacement therapy.

Sex hormone therapy should include estrogens and progestogens in a cyclic regimen or combined estrogen-progestogen preparations. It is preferable to use tri- or biphasic contraceptives that induce cyclic Changes in the endometrium. The Use of estrogen-containing medications serves as prevention against atherosclerosis, osteoporosis, and atrophic processes in the urogenital tract. Young women following total oophorectomy should receive sex hormone preparations until the age of natural menopause (accounting for general contraindications and only if such treatment induces menstruation-like bleeding). Hormone therapy is combined with physiotherapeutic Methods, such as oxygen and carbon dioxide baths, galvanization of the cervicofacial region with a bromine solution, and ultraviolet irradiation sessions.

Premenstrual Syndrome

Premenstrual syndrome (PMS) refers to a distinct set of physical and emotional changes that occur during the second half of the Menstrual cycle and resolve after the onset of menstruation. It affects 20–30% of women of reproductive age. The onset of this syndrome is driven by multiple factors, including progesterone deficiency, Water-Salt METABOLISM disorders, hypersensitivity to endogenous hormones, autonomic nervous system dysfunction, and impaired compensatory responses to metabolic fluctuations throughout the menstrual cycle.

Premenstrual syndrome is characterized by neuropsychiatric symptoms (irritability, depression, tearfulness, insomnia, inappropriate reactions), vasomotor symptoms (headache, precordial pain, tachycardia, hypertension, vegetative-vascular dystonia), and metabolic-endocrine symptoms (pathological weight gain, edema, decreased diuresis, breast tenderness, allergic reactions such as rashes or skin itching). Depending on which symptoms predominate in the clinical picture, the neuropsychiatric, edematous, cephalic, and crisis forms are distinguished.

In mild cases, 3 to 4 symptoms appear 2–10 days before menstruation, with one or two of them being markedly pronounced. They cease with the onset of menstruation. Over the years, the severity of mild premenstrual syndrome remains unchanged. In severe forms, symptoms appear earlier (7–14 days before menstruation), their number is significantly greater (5–12 symptoms), almost all of them are acutely expressed, and they persist until the end of menstruation. Over time, the condition tends to progress, manifested by a shortening of the symptom-free intervals between successive episodes.

Diagnosing PMS requires functional diagnostic tests and assessing the levels of Sex Hormones and prolactin during both Phases of the menstrual cycle. Depending on indications, fluid intake and diuresis monitoring, EEG, mammography, fundus examination, and radiography of the Skull, sella turcica, and cervical spine are performed. Consultations with a neurologist, ophthalmologist, and allergist are recommended.

PMS treatment begins with psychotherapy, establishing a rational daily routine, and proper Nutrition. General massage, water treatments, endonasal electrophoresis with vitamins B₁ and B₆, and electroanalgesia are prescribed. Due to absolute or relative hyperestrogenism, progestogens are indicated (Norcolut 5 mg from day 16 to 25 of the cycle, or according to a contraceptive regimen from day 5 of the cycle for 21 days), while women over 45 are prescribed progestogens in combination with androgens (methylandrostenediol 0.25 g sublingually daily from day 6 to 16 of the cycle). Treatment is supplemented with antihistamines, sedatives, phenothiazine derivatives, and Diuretics. General strengthening therapy, salt and fluid restriction, physiotherapy, and psychotherapy are also necessary.

Premature Ovarian Failure (POF)

POF is a complex of pathological symptoms (Amenorrhea, Infertility, hot flashes affecting the HEAD and upper torso, excessive sweating, etc.) that occur in women under 37–38 years of age who previously had no history of menstrual or reproductive dysfunction.

Premature ovarian failure is a multifactorial condition in which genetic factors play a certain role (chromosomal abnormalities—small congenital ovaries with a depleted follicular apparatus). However, environmental factors play the dominant role (radiation, medications, adverse Pregnancy outcomes, infections, intoxications, hypo- and avitaminosis, stress), leading to damage of the central nervous system and the hypothalamo-pituitary system, followed by gonadal atrophy and replacement with Connective Tissue.

Menarche in patients with POF occurs on time, and menstrual and reproductive Functions remain undisturbed for 12–20 years. The disease typically begins with secondary amenorrhea or oligomenorrhea, and infertility. The characteristic symptoms of this pathology—hot flashes to the head and upper torso, along with sweating—appear 1–2 months after the cessation of menses. These are subsequently joined by irritability, precordial pain, headaches, and decreased working capacity.

All patients with POF have a regular body build and a typically female phenotype. Ovarian dimensions are significantly reduced, which is confirmed by ultrasound data. Their function is markedly suppressed, characterized by a noticeable decrease in estrogen levels alongside elevated gonadotropic hormone levels.

The pupil symptom is always negative, basal body Temperature is monophasic, and the karyopyknotic index (KPI) is 0–10%. Hormonal tests aimed at stimulating ovarian function are negative. Hysterosalpingography reveals a reduction in uterine size and a marked thinning of the mucous membrane in the majority of women. Laparoscopy shows small, wrinkled, yellow ovaries; the corpus luteum is absent, and follicles are not translucent. Histological examination of ovarian biopsies reveals no follicles.

Treatment aimed at stimulating ovarian function is impractical. Women with POF must be prescribed hormone replacement therapy up to the age of physiological menopause and beyond. Preference should be given to preparations containing natural estrogens and progestogens. The latest generation of oral contraceptives may be used in elevated doses. Hormonal drugs are employed to alleviate vasovagal disorders rather than to induce a menstrual-like reaction; therefore, they are used in minimal doses. Treatment is supplemented with general strengthening agents, sedatives, vitamins, and physiotherapy.

Resistant Ovary Syndrome (ROS)

ROS is a complex of pathological symptoms occurring in women under 35 years of age, characterized by amenorrhea (primary or secondary), infertility, normal development of secondary sexual characteristics, macro- and microscopically non-reduced ovaries, and high gonadotropin levels.

There is evidence supporting The Role of iatrogenic factors in The Development of ROS (radiotherapy, cytotoxic drugs, immunosuppressants, as well as ovarian surgeries). Ovarian damage following past tuberculosis, mumps, sarcoidosis, or actinomycosis is quite frequently the cause. The autoimmune theory of ROS development has many proponents, explaining gonadal insufficiency through the blocking action of circulating Antibodies against endogenous gonadotropic hormones on specific FSH receptors in the ovarian tissue. It is also believed that hypothalamo-pituitary dysfunction may contribute to developing ovarian resistance to hormonal action.

In any case, The impact of pathogenic factors results in an inadequate ovarian response to normal or even increased gonadotropin stimulation, manifesting as the following symptoms:

- primary or secondary amenorrhea;

- episodic hot flashes and menstrual-like spotting;

- ovarian hypofunction according to functional diagnostic tests: low cervical index, KPI ranging from 0 to 25%;

- high levels of plasma FSH and LH;

- low levels of plasma estrogens;

- the first progesterone challenge test is most often positive, but subsequent ones are negative;

- a positive response to cyclic estrogen and progestogen therapy or microdoses (1/4 tablet) of combined estrogen-progestogen preparations;

- ultrasound and laparoscopy showing ovaries and Uterus of average size or slightly reduced;

- primordial and preantral follicles detected in ovarian biopsies.

Treating ROS presents significant challenges because the etiopathogenesis of the disease is often undetermined. Consequently, treatment for such patients is quite frequently empirical. There are isolated reports of pregnancies achieved during estrogen therapy. It is believed that the blockade of endogenous estrogens promotes a rebound effect after their withdrawal. Estrogens also increase the number of gonadotropic receptors in the ovaries, thereby potentially enhancing the follicular response to endogenous gonadotropins. There are also isolated reports of a positive effect from cyclic hormone therapy with clomiphene. Data regarding the efficacy of treating ROS patients with gonadotropins remain contradictory.