Заключение
Моноаминовая, хронобиологическая и стрессовая теории развития депрессии получили наибольшее распространение, однако возможны и другие механизмы.
В таблице 1 суммированы некоторые другие возможные патофизиологические гипотезы развития депрессии. Многие из них находятся в тесном взаимодействии или являются частью патогенеза, объясняемого в рамках более известных моделей — нейромедиаторной,стресс-диатезной или нейротрофической. Большинство механизмов описано одновременно при неврологических и психических заболеваниях, что не удивительно, поскольку различные сферы мозговой деятельности, тесно связаны между собой и интегрированы в целостную систему человеческой психики. Кроме того, депрессия также, по-видимому, не является однородным заболеванием и может быть вызвана различными причинами. Эта гетерогенность отражена в современных диагностических критериях, которые пока основаны более на феноменологическом, синдромальном подходе, чем на нозологической, медицинской модели. Об этом, в частности, свидетельствует высокая коморбидность (до 50%) РД с тревожными расстройствами, высокий плацебо эффект (до 50%) и неоднородность эффектов современных антидепрессантов. Искусственное объединение под этим диагнозом весьма различных по клинической картине, течению, патогенезу и реакции на терапию таких состояний, как, например, меланхолическая, атипичная и психогенная депрессия или депрессии, протекающие с преобладанием идеомоторной заторможенности (ступорозности), тревоги или психической анестезии, затрудняет поиск биологической основы этих состояний и более эффективных дифференцированных методов терапии. Очевидно, что при развитии заболевания в молодом возрасте существенную роль играют генетические факторы и, возможно, ранние стрессовые воздействия. В зрелом и старшем возрасте большее значение приобретают хронический стресс, нарушения хронобиологических процессов и коморбидные соматические заболевания. Кроме того, при рекуррентном и хроническом течении депрессии отмечаются когнитивные расстройства, нарушается социальная адаптация и развиваются нейродегенеративные изменения. Очевидно также, что у большинства больных депрессией нарушается сон и наблюдается десинхронизация циркадианных ритмов, а также ритмов другой периодичности, что может быть главным патофизиологическим звеном депрессии. Хотя каузальная связь между этими нарушениями и РД пока не установлена, хронотерапевтическая стратегия уже должна учитываться в комплексной терапии депрессивных больных, поскольку может обеспечить более высокую эффективность не только в отношении полноценной редукции симптоматики, но и в обеспечении профилактического эффекта и достижении более высокого уровня социального функционирования и качества жизни.
Отсутствие единой стройной теории развития депрессии стимулирует наш исследовательский интерес, который в последние годы направлен на поиск более точных биологических маркеров заболевания и новых методов лечения.
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