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Таблица № 1. Сравнительный анализ двух групп детей по международным шкалам
Кол-во детей Шкала спастичности по Эшворту GMFCS 100% психо-эмоциональная шкала
При пост. При вып. Ср. показ. При пост. При вып. Ср. показ. При пост. При вып. % улучш.
Дети, получившие БТА
74 3,1 2,2 0,9 3,6 2,8 0,8 56,7 64,6 7,9
Дети, не получившие БТА
23 2,3 1,5 0,8 2,9 2,1 0,8 66,5 74,8 8,3
В сравнительном аспекте у детей, получивших БТА, отмечается больший процент улучшения по шкалам Эшворта и 100% психоэмоциональной шкале, что свидетельствует об эффективности применения данного препарата в комплексной реабилитации.
Наряду с ЛФК и лекарственной терапией широко применяется и аппаратное лечение. Это такие высокотехнологичные инновационные разработки как постурография, БОС опорно-двигательный, БОС психо-эмоциональный, БОС
логопедический.
Таким образом, при реабилитации детей со спастико-гиперкинетической формой заболевания используются все передовые технологии, применяемые в мировой практике. Более того, как правило, не существует четко определенной схемы. Для каждого пациента подбирается индивидуальная программа реабилитации с учетом всех психических, психологических, физиологических возможностей и особенностей.
литература:
1. Шамарин Т.Г., Белов Г.И. Возможности восстановительного лечения детских церебральных параличей. - Элиста: Джангар. - 1999. - 168 с., ил.
2. Зверева З.В. Патогенетические механизмы реабилитации (абилитации) и патогенетическая симптоматическая фармакотерапия при детском церебральном параличе //Журн. Практика педиатра. - 2010. - С. 56-61.
3. Семенова К.А.Восстановительное лечение больных с резидуальной стадией детского церебрального паралича. - М.: «Антидор», 1999. - 384 с.
4. Физическая реабилитация детей с нарушениями функций опорно-двигательного аппарата / Под ред. Н.А. Гросс. - М.: Советский спорт, 2000. - 244 с.
5. Статистические данные психоневрологического отделения «Акжол» АО «<РДРЦ» за 20102011 годы.
Материал поступил в редакцию 29.06.2012 г.
U.D.C. 618
K.A. Abasheva
Shalkar district hospital, Aktobe, Kazakhstan
PREMENSTRUAL SYNDROME
Premenstrual syndrome or (premenstrual tension, cyclic syndrome) is a cyclic symptom complex which occurs at some women during premenstrual days (for 2 up to 10 days before menstruation) and is characterized by psycho-emotional, vegetative-vascular and metabolic endocrine disorders which, in turn, have a negative impact on the usual way of life of women [1,3].
The characteristic feature of clinical course of PMS is a rhythm of its manifestation which may
be associated with the luteal phase of the cycle in regularly menstruating women, and have a certain frequency in patients with menstrual disorder as well as inability to trace cyclicism of ovarian functioning (after hysterectomy without appendages), at puberty or perimenopause [5, 7-11].
The frequency of premenstrual syndrome depends entirely on the woman's age: the older woman -the more frequency, it ranges from 25 to 90%. At the age from 19 to 29 years PMS is
observed at 20% of women, at the age of 30 years and more the syndrome occurs in about every other woman. At the age of 40 years and more the frequency comes up to 55%. PMS is frequently occurs at emotionally labile women having lack of body mass and intellectual work. Triggering factors such as delivery and abortion, mental stress and infectious diseases also have influence on the onset of symptoms of cyclic syndrome. PMS occurs more often in women with disorders of the central nervous system, gastrointestinal tract, and cardiovascular system, and can be observed in the ovulatory cycle (the cycle in which ovum releases from the ovary into the body cavity), and in an ovulatory (cycle in which there is no release of an ovum) [2].
Hormonal therapy. In 1931, Robert Frank reported that PMS was caused by estrogen and progesterone ratio disorder in the luteal phase of the menstrual cycle (MC). Excess of the first hormone and lack of the second one leads to the development of symptoms such as headache, adynamia, tiredness, and diuresis decrease. The reason is that a large amount of estrogen causes hypoglycemia, which is characterized by a feeling of tiredness, and lack of progesterone leads to fluid retention [5,6]. The bottom-line of hormonal theory is the following thesis: "PMS does not exist without ovarian activity," i.e., pre-menstrual syndrome cannot occur before puberty, after menopause, during pregnancy and in women who have no ovaries [4].
Currently, there are some studies which prove that women' hormones at PMS don't change. Therefore, we can assume that the premenstrual syndrome develops not only because of lack of progesterone, but also because of the characteristics of its metabolism in the CNS. In the normal metabolism, progesterone can form allopregnanolon that stimulates GABA-A receptors, and increases the activity of chloride ion tubules of neural membranes, providing sedation effect. When disorders of progesterone metabolism in CNS, the hormone produces pregnanolon which is an antagonist of the A and B GABA receptors, which may explain the presence of clinical symptoms of PMS. Pregnanolon also can cause depression which occurs at premenstrual syndrome. Moreover, the hormonal theory of PMS' presence studies androgen content changes (such as testosterone, androstenedione, and others), corticosteroids, and hyperproduction of posterior and middle lobe of the pituitary [9].
According to allergic theory, premenstrual syndrome is a result of hypersensitivity to endogenous progesterone. We can prove its presence using positive skin test with sex steroid hormones in the luteal phase of the menstrual cycle [9].
The theory of "water intoxication" states that the fluid retention in patients with PMS is caused by neuroendocrine disorders, such as changes in the system "of the renin-angiotensin-aldosterone system". It is suggested that hypersecretion of adrenocorticotrophic hormone by pituitary under the stress and increase of high level of serotonin and angiotensin II hormones affects increasing of aldosterone formation. Angiotensinogen, in turn, is secreted by the liver under the influence of estrogen, and renin is an enzyme that converts angiotensinogen to angiotensin [11].
Hyperadrenocortical activity and aldosterone increasing theory hypothesizes that estrogen can increase the level of plasma rennin by increasing of angiotensinogen by liver, and therefore, increases the activity of renin and angiotensin II hormones, which leads to an excess of aldosterone. In turn, progesterone increases rennin activity, thereby increases the secretion and excretion of aldosterone. Thus, at aldosteronism there is absorption of sodium in the renal tubules, which causes potassium and calcium lost and fluid accumulation in the tissues, and progesterone is an aldesterone's antagonist, hence for, its failure may develop secondary hyperaldosteronism [3].
The most modern theory of PMS origin is the theory of "metabolic neurotransmitter in the central nervous system." According to this hypothesis, premenstrual syndrome can be viewed as a functional disorder of the central nervous system because of external factors to congenital or acquired hypothalamic-lability hypothalmic-pituitary-ovarian system [2].
In recent years, the pathogenesis of PMS has begun to pay much attention intermedia pituitary peptides: melano- stimulating hormone. This hormone is influenced by sex steroids, and the interaction with endorphin may cause to mood changes. Endorphins may also cause changes in mood, behavior, increase appetite and thirst. In some cases, endorphins may cause increased levels of prolactin, vasopressin and their inhibitory effect on the action of prostaglandin E may be engorgement, constipation, fluid retention and bloat [7].
Among other things, the development of premenstrual syndrome may be associated with the presence of vitamin deficiency in the luteal phase of the menstrual cycle [9].
We should also focus on changeable PMS which is manifested by emergence or intensification of cyclic symptoms (even in the absence of regular MC) under the influence of the hormonal change in premenopause, which may eventually go into climacteric syndrome [5, 7, 12].
Taking into account the variability and the
large number of heterogeneous PMS events, when its diagnosis we should proceed, first and foremost, not the analysis of symptoms per se, but from the presence of cycles in the manifestation of symptoms. The particular importance of this stage takes in cases where there is no regular MC at the surveyed women. The heart of diagnostic search is a detailed analysis of the history, as well
as application of the method of self-observation -the patient's diary with notes about the presence and intensity of premenstrual disorder during 2-3 months [6, 7, 10, 13].
Currently, the diagnosis of PMS pays great attention to the methods of endocrine status.
The following criteria for differential diagnostics was proposed.
Table I.Criteria for differential diagnostics of premenstrual disorders
Symptoms PMS Premenstrual Dystrophic Disorders
Fluid retention Low physical discomfort Criteria: 5 from 11 symptoms (including
Puffiness At least one of the four):
Mass Increasing Fluid retention / Puffiness Depressive state
Increased Appetite Anxiety
Irritability Mammary glands tenderness Mood swings
Mammary glands tenderness (mammalgia) Aggression, passing into irritability
Increased Appetite
Mass increasing
Bad concentration Bad concentration
Tiredness
Irritability (at absence of Premenstrual Dystrophic Disorders criteria) Appetite change
Insomnia/drowsiness
Self-control disorder
Criteria absence Mastalgia, joint pains,
Premenstrual Dystrophic Disorders edemas, mass increasing
Adjuvant hormonal researches apply methods of determining the functional state of the thyroid gland (TSH, T3, T4), serum concentrations of cortisol, C-peptide, sex steroid binding globulin, glucose tolerant test.
Status of hormone producing ovarian function is studied also by ultrasound study of genitals on the base of their morphological characteristics (biometrics, quality and value of follicular unit and the stroma, and state folliculogenesis) and uterus (endometrial thickness and quality, the structure of the myometrium).
Our studies have shown the critical importance of exclusion of chronic inflammatory diseases of the
genitals, especially Candida and viral etiology, in the process of identifying the causes of premenstrual disorders, including PMS. For this purpose, it is advisable to carry out a survey to identify infections, sexually transmitted diseases, as well as dysbiosis.
Additional methods of the research shall be applied depending on the type and primary clinical aspects of premenstrual disorders. They include ECG, EET, MRI of head, USI of thyroid gland and lacteal glands, mammography, antropometric researches (definition of body mass index: BMI = weight (kg)/height(m)), definition of dieresis, excretory kidney function [2, 5, 7, 9, 14].
We adhere to the following PMS drug therapy.
Table 2
Drug groups. Pathogenetic basis and their activity Drugs. Recommended doses and application modes
Drugs regulating blood supply, metabolism and functional condition of the CNS
Improvement of microcirculation and metabolic processes in the CNS in order to stabilize pituitary-hypothalamic ovarian system Nootropic effect Psychotropic effect (sedative, anxiolytic, thymoleptic) Sleep normalization 1. MagneB6 1-2 tablets x 3 times per day 2. Helarium Hypericum 1 tablet 3 times per day 3. Piracetam 0.4-1.2 g per day 4. Instenon 1 tablet 3 times per day
Vasoactive drugs
Normalization of hemorheology Regulation of vascular tone Angioprotective effect Improvement of organs and tissue blood supply Secondary analgesic effect (due to decrease of hydrophilia of bone marrow tissues) Memoplant, billobil 1-2 tablets 3 times per day Troxerutin 1 tablet 3 times per day Pentoxifylline 100.0-300.0 mg per day Drugs containing polyunsaturated fatty acids and multivitamins
Drugs of neuromediator effect
Normalization of prolaktine production Extract Vitex agnus castus (mastodinon, ciclodinon) Serotoninergic effectHOH по 20-40 капель 3 раза в день) Psychotropic activity Erbisol 1.0 ml i.m. daily No. 30 Ubiquinone 2.2 ml i/m 1 time in 3 days No. 10 Coenzyme-compositume 2.2 mm i/m 1 time in 3 days No.10 Aktovegin 2.0 i.m. daily No.10
Hormonal drugs
They shall be assigned in accordance with detected disorders of hormonal homeostasis individually in each case.
Gestagens
Progestogenic, antiandrogenic, antimineral and corticoid effect Утрожестан 200,0 мг в сутки с 16-го по 25-й Dyufaston 20.0 mg per day from the 16th day to the 25th MC
день Normalization of neurosteroid change in the CNS . МЦ Utrozhestan 200.0 mg per day from the 16th day to the 25th MC
Combined oral contraceptives
Exclusion of ovulation and lutein phase of the MC Ethinylestradiol (30.0 mkg) — drospirenone (3.0 mg) Ethinylestradiol (30.0 mkg) — dienogest (2.0 mg) Ethinylestradiol (30.0 mkg) — gestodene (0.75 mg)
Agonists of dopamine receptors
Normalization of prolaktine production Бромокриптин 2,5-7,5 мг в сутки Neuromediator effect Достинекс 5,0 мг в неделю во II фазу МЦ Bromokriptine 2.5-7.5 mg per day Dostinex 5.0 mg per week in the 2nd phase of the MC Extract Vitex agnus castus (mastodinone, ciclodinone 20-40 drops 3 times per day)
Agonists of gonadotropic releasing hormones
Reversible temporary decrease of production of steroid hormones in gonads Buserine 3.75 mg i/m 1 time per 28 days or spray 900.0 mkg per day 1-3 months Difereline 3.75 mg i/m 1 time per 28 days No. 1-3
Normalization of work-rest ratio with a good sleep and graduated exercises shall be obligatory
at treatment of PMS. Recommendations concerning food ration shall be made considering principles of healthful and dietary meals at the PMS [5]: controlled calorage (1200-1500 kkal/day); divided nutrition regimen (5-6 times per day); exclusion or decrease of eating several products, including products with high content of salt, coffein, simple carbohydrates, saturated fatty acids, preservation agents, and smoked food; addition of vitamins, microelements, and polyunsaturated fatty acids to the ration.
Currently, disorder of neurochemical regulation of cerebral systems is considered as a trigger mechanism in the genesis of neurometabolic and endocrine syndromes, to which PMD is referred [14, 8]. Thus, normalization of biochemical processes in the bone marrow tissue is appropriate at all variants of PMS courses by application of drugs regulating blood supply, metabolism and functional condition of the CNS. Primarily, it is necessary to lay emphasis on herbal drugs with sedative, anxiolytic and antidepressant action. Thus, helarium giperikum has expressed and long clinical effect in reducing of PMS signs at assignment of middle therapeutic doses (1-2 tablets for three times per day) in the phase II or in continuous mode at the severe forms.
Among the drugs of special effect, it is necessary to lay emphasis on the group of nootropics which contribute in strengthening, general activity of a woman, stabilization of psychoemotional sphere by strengthening metabolic and electrophysiological processes and intensification of cerebral circulation.
Normalization of dopamine exchange is another important mechanism of regulation of neuroendocrinal disorders at the PMS. [1,2,4,10,11].
Drugs containing derivatives of Vitex agnus castus (mastodinon - 20-30 drops or 1-2 tablet 3 times per day, ciclodinone - 40 drops or 1 tablet, similarly) as well as ergoline derivatives bromokriptin and dostinex keep neurochemical balance in tuberoinfundibular system in the CNS by connecting with B2 receptors. Accordingly, when assigning them it is necessary to proceed from presence of absolute increase of serum level of prolaktin and such clinical signs as a headache, giddiness, disorientation, nausea, vomit of central genesis and/or mastalgia.
At middle severe and severe forms of the PMS it is necessary to include drugs improving trophic processes and having immunocorrecting and adaptogenic effect.
Gestagenic therapy is shown in the complex of treatment of the PMS at insufficiency of lutein phase of the cycle. At selection of a drug, it is necessary to estimate its progestogenic activity and presence or absence of interaction with other receptors of the steroid hormones which can be both useful and undesirable in the context of PMS treatment.
At severe forms of the PMS, it is necessary to apply drugs providing reversible pharmacological exclusion of ovarium except for above-mentioned non-hormonal drugs - agonists of gonadotropic releasing hormones with further prescription of the mentioned COC.
Thus, in the result of the conducted survey of available literature, we concluded that PMS is a multiple form of women's pathology requiring attentive and specific diagnostics and treatment of each case.
References
I. V.I. Kulakov. Clinical recommendations. Obstetrics and gynecology. Publication 2. — Moscow: GEOTAR-Media, 2008. — P. 368—377. — 543 p. — 3000 copies. V.M. Cattile, R.A. Arki Edited by Prof. V.N. Prilepskaya Polyclinic gynecology. — Moscow: MEDpress -inform, 2005. — P. 302—325. — 640 p. — ISBN 5-98322-1042. Ph. Khukho. Neurochemistry. Basis and principles.— M.: Mir,
3. 1990.— 384 p.
4. Reference of clinical neurovegetology/ Edited by V.A. Berseneva— K.: Health, 1990.— p. 364 .
5. V.E. Radzinskiy. Guidelines for practical work on gynecology - Moscow: Medical and informative agency, 2005 - P.142-149-520 p. - 3500 copies - ISBN 5-89481-3046. L.N. Vassilevskaya, V.I. Grishenko, V.I. N.A. Sherbina, V.P. Yurovskaya. Gynecology - Rostov-on-
Don: Fenix, 2002 - p - 189-193, 576 p - (Textbooks, work-books) - 10,000 copies - ISBN 2-22202814-2.
7. Deuster P.A., Tilahum A. Biological, social and behavioural factors associated with PMS // Arch. Fam. Med.— 1999.— No. 8.— P. 122-128.
8. I.B. Manukhin, L.G. Tumilovich, M.A. Gevorkyan. Clinic lectures of gynecologic endocrinology - M.: MIA, 2001 - p 247.
9. J. Martorano,A.Morgan, U. Freir Premenstrual syndrome: Translation from English - S. Pb.: Set, 1998 - p. 217.
10. T.A. Serova, Woman's health: menstrual cycle and hormones in classical and unconventional medicine - Rostov-on-Don, 2000 - p. 416.
II. Loch E, Selle H., Boblitz N. Treatment of PMS with Phytopharmaceutical Formulation Containing
Vitex agnus castus // J. of Women's Health.— 2000.— Vol. 9, No.3.— P. 315-320.
12. The Premenstrual syndrome in different age groups / T.F. Ta-tarchuk, J.P. Solsky, T.V. Shevchuk et al. // Climact. J. of the Intern. Menopause Soc.— 1999.— Vol. 2 (suppl. 1).— P. 163.
13. V.P.Smetnik, V.G. Tumilovich. Non-operative gynecology: Guidelines for doctors - M.: MIA, 1998-p.592
14. Freeman E. Treatment of severe PMS // JAMA.— 1995.— No. 51.— P. 54.
15. Frank R.T. The hormonal causes of premenstrual tension // Arch. Neurol. Psychiatry.— 1931.— № 26.— P. 1052-1057.
16. Studd J., Cronje W. Transdermal estrogens for the treatment of PMS // Adv. In Gyn. Endocrin.— 2000.— No. 4.— P. 83-89.
Material Received by the Editors 12.08.2012.
УДК: 616.831-009.11-053.2 Б.С. Кененбаева
«Республикалык, балалар оцалту орталыгы» АК, Астана каласы, Казакстан
БАЛАЛАР ЦЕРЕБРАЛДЫ САЛ АУРУЫ ЖЭНЕ ОНЬЩ ТYРЛЕРI
Балалар церебралды салдануы (БЦС) -курсанта даму кезшде, туу кезшде жэне туган сэтте байкалатын бас ми ауруы. Бул ауру кеп жылдар агымында, кебшесе бYкiл емiр бойында жалгасады.
Балалар церебралды салдануы 8ртYрлi экономикалык зияндыктардан, эмбрион тукымга немесе жача туган н8рестеге 8сер етушен пайда болады. ^имыл-козгалыс бузылулары - салда-ну, парез, ершаз кимылдар, атаксия т.б.; сейлеу кабiлетi мен психикалык бузылулары БЦС клиникалык суреттемесiне жатады. БЦС-ныч клиникалык керсетiлiмдерi полиморфты, олар мидыч патологиялык даму кезендегi езгерiстерiне байланысты.
Моториканыч толык дамымауы мен патологиялык даму уштастьнында 8сiресе мачызды ж8не киын болатыны булшык ет тону-сы регуляциясыныч бузылысы: ол спастикалык, ригидтiк, дистониялык, гипотониялык тYPде кездеседi. Булшык ет тонусы регуляциясыныч бузылуы, 8сiресе аурудыч алгашкы с8ттерiнде, тоникалык ж8не нускаулык рефлекстердiч патологиялык дамыумен, осы непзде патологиялык синергияныч калыптасуымен байланысты.
Аурудыч аскыну барысында осы бузылулардыч непзшде булшык еттер, CYйектер, буындар кайта езгерiстерге ушырайды: сiресулер, ыдырау, сколиоз бен кифосколиоз пайда болады ж8не патологиялык козгалыстар стереотипi калыптасады.
Мидыч даму патологиясы мен тежелуi психикалык дамудыч бузылуына 8сер етедi. ЭртYрлi авторлардыч м8лiметтерiне караганда, психикалык дамудыч тежелуi БЦС-пен ауыратын балалардыч 40-50 % курайды, олигофрениямен
ауратын балаларда 20-25 % курайды, тек кана 20-25 % балаларда интеллект калыпты дамуы байкалады, ал 75 % балаларда сейлеу кабтеп 8ртYрлi формада бузылган.
БЦС-ныч сауыктыру терапиясыныч кYPделi комплексiне: д8рiлiк терапия, сейлеу кабтеп мен танып бiлудi калыптасты жумыстары, емдiк дене шыныктыру, массаж, ортопедиялык режим, ортездеу, протездеу, педагогикалык коррекция жумыстары: логопед, дефектолог, психолог, ойын, ечбек, 8н-кYй терапия ж8не жача инновациялык технологиялык 8дiстер: роботталган кинезотера-пия, биологиялык керi байланыс (БКБ) кимыл-^рек, психо-эмоционалды, логопедия тренингтерi, кажет болса хирургиялык емдеу ж8не физиотерапиялык емдеу мен жергiлiктi булшык ет релаксанты: «А» типт ботулотоксин мредк
Бул емдеу тYрлерiнiч барлыны сауыктыру терапиясыныч мачызды элементтерi болып та-былады, бiрак олардыч м8нi ею шартты сактауга байланысты.
Бiрiншiден: мидыч дамуын жуйелеуге багытталган д8рiгерлiк терапия жасау, жуйке талшыктарын миелинизациялау процессiн жуйелеу. Д8рiгерлiк терапия 8р жаедайда 8ртYрлi болуы керек; аурудыч тYрiне, кезечше, баланыч соматикалык жаедайына байланысты.
Екшшщен: козгалыс функцияларын, психикалык ж8не сейлеуд калыптастыру жумыстарын 8р уакытта туракты ж8не жYйелi тYPде еткiзу керек.
I. ^аз1рп уакытта БЦС-ныч бiртутас клас-сификациясы жок. Кеп жылдар бойы козгалыс бузылулары БЦС-ныч еч орталык звеносы болып каралды, оныч жеке тYрлерi классификациясы топографиялык принцип бойынша каланды: те-
