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000186564 0247_ $$2doi$$a10.1111/jcpp.12384
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000186564 037__ $$aFZJ-2015-00637
000186564 041__ $$aEnglish
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000186564 1001_ $$0P:(DE-HGF)0$$aFirk, C.$$b0$$eCorresponding author
000186564 245__ $$aImplicit sequence learning in juvenile anorexia nervosa: Neural mechanisms and the impact of starvation.
000186564 260__ $$aMalden$$bBlackwell Publishing Limited$$c2015
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000186564 520__ $$aBackgroundPrevious studies have reported that cognitive deficits occur in patients with anorexia nervosa (AN) and that these deficits may represent a predisposition towards developing AN or perpetuate the disorder. Specifically, dysfunctional implicit learning may contribute to the development of highly resistant dieting behaviours that are fundamental to the persistence of the disorder. Thus, the aims of this study were (a) to investigate implicit sequence learning in adolescent patients with AN before and after weight recovery and (b) to elucidate the associated neural mechanisms in acute AN relative to healthy controls.MethodsIn a behavioural study, implicit sequence learning was assessed using a serial reaction time task in 27 adolescents with AN before (T1) and after weight recovery (T2) compared with age-matched healthy controls (HC) who were assessed at similar time intervals. The neural correlates of implicit sequence learning were subsequently investigated in 19 AN patients shortly after they were admitted to the hospital and 20 HC using functional magnetic resonance imaging (fMRI).ResultsAt T1, AN patients showed reduced sequence learning compared with HC. However, no behavioural differences between HC and AN patients were found at T2. At the neural level, acute AN patients showed reduced thalamic activation during sequence learning compared with HC subjects.ConclusionsOur data suggest that the impaired implicit learning observed in adolescent AN patients before weight gain is a state-related dysfunction that normalises with weight gain. Thus, implicit learning deficits do not appear to represent a predisposition towards developing AN; rather, these deficits should be considered when planning psychotherapeutic interventions for acute AN. Reduced thalamic activation during the acute stage of AN may indicate a starvation-induced dysfunction of the neural circuitry that is involved in behavioural flexibility.
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000186564 7001_ $$0P:(DE-HGF)0$$aMainz, V.$$b1
000186564 7001_ $$0P:(DE-Juel1)131741$$aSchulte-Rüther, M.$$b2
000186564 7001_ $$0P:(DE-Juel1)131720$$aFink, G. R.$$b3
000186564 7001_ $$0P:(DE-HGF)0$$aHerpertz-Dahlmann, B.$$b4
000186564 7001_ $$0P:(DE-HGF)0$$aKonrad, K.$$b5
000186564 773__ $$0PERI:(DE-600)2255259-5$$a10.1111/jcpp.12384$$n11$$p1168-1176$$tJournal of Child Psychology & Psychiatry$$v56$$x0021-9630$$y2015
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