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<article article-type="review-article" dtd-version="1.3" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xml:lang="ru"><front><journal-meta><journal-id journal-id-type="publisher-id">medsovet</journal-id><journal-title-group><journal-title xml:lang="ru">Медицинский Совет</journal-title><trans-title-group xml:lang="en"><trans-title>Meditsinskiy sovet = Medical Council</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">2079-701X</issn><issn pub-type="epub">2658-5790</issn><publisher><publisher-name>REMEDIUM GROUP Ltd.</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.21518/ms2026-086</article-id><article-id custom-type="elpub" pub-id-type="custom">medsovet-9971</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="ru"><subject>ДЕТСКАЯ НЕВРОЛОГИЯ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>CHILD NEUROLOGY</subject></subj-group></article-categories><title-group><article-title>Астеническое расстройство у детей и подростков: вопросы диагностики и патогенеза</article-title><trans-title-group xml:lang="en"><trans-title>Asthenic disorder in children and adolescents: Aspects of diagnosis and pathogenesis</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-4276-8400</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Нестеровский</surname><given-names>Ю. Е.</given-names></name><name name-style="western" xml:lang="en"><surname>Nesterovskiy</surname><given-names>Yu. E.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Нестеровский Юрий Евгеньевич - к.м.н., доцент кафедры неврологии, нейрохирургии и медицинской генетики имени академика Л.О. Бадаляна Института нейронаук и нейротехнологий.</p><p>117997, Москва, ул. Островитянова, д. 1</p></bio><bio xml:lang="en"><p>Yuriy E. Nesterovskiy - Cand. Sci. (Med.), Associate Professor of the Department of Neurology, Neurosurgery and Medical Genetics named after Academician L.O. Badalyan, Institute of Neurosciences and Neurotechnology, Pirogov Russian National Research Medical University.</p><p>1, Ostrovityanov St., Moscow, 117997</p></bio><email xlink:type="simple">yenest@bk.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Российский национальный исследовательский медицинский университет имени Н.И. Пирогова</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Pirogov Russian National Research Medical University</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2026</year></pub-date><pub-date pub-type="epub"><day>19</day><month>04</month><year>2026</year></pub-date><volume>0</volume><issue>3</issue><fpage>137</fpage><lpage>144</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Нестеровский Ю.Е., 2026</copyright-statement><copyright-year>2026</copyright-year><copyright-holder xml:lang="ru">Нестеровский Ю.Е.</copyright-holder><copyright-holder xml:lang="en">Nesterovskiy Y.E.</copyright-holder><license xml:lang="ru" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>Данная работа распространяется под лицензией Creative Commons Attribution 4.0.</license-p></license><license xml:lang="en" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>This work is licensed under a Creative Commons Attribution 4.0 License.</license-p></license></permissions><self-uri xlink:href="https://www.med-sovet.pro/jour/article/view/9971">https://www.med-sovet.pro/jour/article/view/9971</self-uri><abstract><p>Астеническое расстройство у детей и подростков является полиэтиологическим состоянием, характеризующимся развитием разнообразной клинической картины с доминирующей жалобой на повышенную утомляемость и быструю истощаемость, как психическую, так и физическую, носящие устойчивый и длительный характер. По данным литературы, обращаемость за медицинской помощью в связи с астеническими симптомами достигает 64%. Распространенность астенического расстройства у детей и подростков определить крайне сложно, т. к. многочисленные клинические симптомы часто рассматриваются в контексте других заболеваний, а не как одно самостоятельное патологическое состояние. В основе развития этого состояния лежат труднодифференцируемые между собой нарушения как функционального, так и органического характера, возникающие вторично на фоне другой разнообразной патологии. Одним из ведущих механизмов развития астенического синдрома является нарушение функционирования ретикулярной формации (ретикулярной активирующей системы – РАС). Выраженные проявления астенического расстройства, приводящие к существенному нарушению повседневной активности и значительно снижающие качество жизни пациента на протяжении более 6 мес., рассматриваются как отдельная нозологическая форма заболевания – синдром хронической усталости (СХУ). Считается, что в развитии СХУ могут быть задействованы гены, регулирующие работу оси «гипоталамус – гипофиз – надпочечники», которая отвечает за реакцию организма на стресс. Сбой в функционировании одного из компонентов этой системы может нарушить работу всей системы и способствовать развитию повышенной утомляемости. Астенические расстройства являются одним из частых симптомов у пациентов, перенесших черепномозговую травму. Одним из маркеров повреждения и процессов восстановления нервной ткани при черепно-мозговой травме является N-ацетиласпартат (NAA). Большой интерес представляют исследования, посвященные роли NAA в развитии астенических расстройств. Метод МР-спектроскопии головного мозга позволил обнаружить определенные нейрохимические аномалии, потенциально подлежащие лечению с помощью препаратов, влияющих на выявленные в центральной нервной системе метаболические нарушения. Поиск новых физиологических и биохимических маркеров астенического синдрома расширит представления о патогенезе и возможностях лечения данных состояний.</p></abstract><trans-abstract xml:lang="en"><p>Asthenic disorder in children and adolescents is a polyetiological condition characterized by a varied clinical picture with the dominant complaint of increased fatigue and rapid exhaustion, both mental and physical, which are persistent and last for a long period of time. It is reported that medical aid appealability rates due to asthenic symptoms achieve up to 64%. The prevalence of asthenic disorder in children and adolescents is extremely difficult to determine, as the numerous clinical symptoms are often viewed within the context of other diseases rather than as a single, hallmark pathology. The development of this condition is driven by challenging-to-differentiate functional and organic disorders that arise secondary to other, diverse pathologies. Dysfunction of the reticular activating system (RAS) is one of the primary mechanisms underlying asthenic syndrome. Severe manifestations of asthenic disorder which result in the significant impairment of daily activities and considerable deterioration of the patient's quality of life for more than 6 months are considered as a separate nosological entity — chronic fatigue syndrome (CFS). Genes regulating the hypothalamic-pituitary-adrenal (HPA) axis that is the body's main way of responding to stress are believed to be involved in the development of CFS. A single component failure can disrupt the entire system and contribute to the development of increased fatigue. Asthenic disorders are one of the common symptoms in patients who have suffered a traumatic brain injury (TBI). N-acetylaspartate (NAA) is seen as one of the markers of nerve tissue damage and repair in traumatic brain injury. Research on the role of NAA in the development of asthenic disorders is of great interest. Brain magnetic resonance spectroscopy (MRS) has found specific neurochemical abnormalities that can potentially be treated with agents targeting metabolic disturbances identified in the central nervous system. The search for new physiological and biochemical markers of asthenic syndrome will expand our understanding of the pathogenesis and treatment options for these disorders.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>астения</kwd><kwd>астеническое расстройство</kwd><kwd>астенический синдром</kwd><kwd>патологическая утомляемость</kwd><kwd>синдром хронической усталости</kwd><kwd>посткоммоционный синдром</kwd><kwd>биомаркеры</kwd><kwd>N-ацетиласпартат (NAA)</kwd><kwd>лечение</kwd><kwd>N-ацетиламиносукцинат</kwd><kwd>дети</kwd><kwd>подростки</kwd></kwd-group><kwd-group xml:lang="en"><kwd>asthenia</kwd><kwd>asthenic disorder</kwd><kwd>asthenic syndrome</kwd><kwd>pathological fatigue</kwd><kwd>chronic fatigue syndrome</kwd><kwd>post-concussion syndrome</kwd><kwd>biomarkers</kwd><kwd>N-acetylaspartate (NAA)</kwd><kwd>treatment</kwd><kwd>N-acetylaminosuccinate</kwd><kwd>children</kwd><kwd>adolescents</kwd></kwd-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Захарова ИН, Творогова ТМ, Пшеничникова ИИ, Сгибнева АИ. 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