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2017 | 17 | 3 | 216–224
Article title

Anhedonia w zaburzeniach depresyjnych

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EN
Anhedonia in depressive disorders
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PL
Abstracts
EN
Although anhedonia may be a component of the clinical picture in many mental and neurological conditions, it is one of the most common and typical negative symptoms observed in depressive episodes. Both, the baseline increase in the severity of anhedonia as well as its regression during treatment are strong predictors of the efficacy of antidepressant pharmacotherapy and can have a significant impact on patient’s ability to achieve functional remission. Nevertheless, studies on the effects of antidepressants on the possible reduction of anhedonia-spectrum symptoms are very sparse. Depressive anhedonia-like emotional disorders, which are considered by patients to be associated with the inclusion of an antidepressant (usually from the class of serotonin or serotonin–noradrenalin reuptake inhibitors) and often experienced as qualitatively different from the former, are another clinical issue. Although they may be beneficial in some cases by helping the patient release anxiety and depressive symptoms, they are often seen as adverse effects eliminating the emotional intensity and social interactions. It is believed that depressive anhedonia and emotional disorders associated with antidepressant therapy have similar neurobiological mechanisms and result from the reduced activity (particularly in the form of reduced dopaminergic transmission) of reward system structures, such as the prefrontal cortex or the ventral tegmental area. Agomelatine is an antidepressant with the best documented and proven efficacy in reducing the increased depressive anhedonia and the lowest potential to cause drug-induced anhedonia. This may be due to its specific pharmacodynamic properties and, most of all, the ability to potently block the postsynaptic 5-HT2C receptors, which results in the enhancement of dopaminergic and noradrenergic transmission.
PL
Anhedonia bywa elementem obrazu klinicznego wielu zaburzeń psychicznych i neurologicznych, jednak najczęściej i w sposób najbardziej typowy występuje w przebiegu epizodu depresyjnego, jako jeden z jego osiowych objawów. Zarówno wyjściowe nasilenie anhedonii, jak i jej ustępowanie w trakcie leczenia są silnymi predyktorami skuteczności farmakoterapii przeciwdepresyjnej i mogą znacząco wpływać na możliwość osiągnięcia przez pacjenta remisji funkcjonalnej. Mimo to wpływ leków przeciwdepresyjnych na możliwość redukcji nasilenia objawów należących do spektrum anhedonii bardzo rzadko był dotąd przedmiotem badań. Odrębnym zagadnieniem klinicznym jest zespół podobnych do anhedonii depresyjnej zaburzeń emocjonalnych, które są przez chorych kojarzone z włączeniem leku przeciwdepresyjnego (zazwyczaj z grupy inhibitorów wychwytu zwrotnego serotoniny lub serotoniny i noradrenaliny) i często doświadczane jako odmienne jakościowo od tej pierwszej. Niekiedy mogą być korzystne i stanowić formę uwalniania pacjenta od objawów lękowych i depresyjnych, ale też często postrzegane są jako uciążliwe działania niepożądane, odbierające intensywność życia emocjonalnego oraz interakcji społecznych. Uważa się, że anhedonia depresyjna i zaburzenia emocjonalne kojarzone z leczeniem przeciwdepresyjnym mają podobne podłoże neurobiologiczne i wiążą się ze spadkiem aktywności (zwłaszcza w postaci osłabienia transmisji dopaminergicznej) struktur związanych z układem nagrody, takich jak kora przedczołowa czy rejon brzuszny nakrywki. Lekiem przeciwdepresyjnym o najlepiej udokumentowanej i udowodnionej skuteczności w zakresie redukcji nasilenia anhedonii depresyjnej oraz o najmniejszym potencjale wywoływania anhedonii polekowej jest agomelatyna. Mogą o tym decydować jej specyficzne właściwości farmakodynamiczne, a przede wszystkim zdolność do silnej blokady postsynaptycznych receptorów 5-HT2C, której efektem jest torowanie transmisji dopaminergicznej i noradrenergicznej.
Discipline
Year
Volume
17
Issue
3
Pages
216–224
Physical description
References
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article
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bwmeta1.element.psjd-a30c4ec2-c812-45aa-a784-6711ca8faf53
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