Source Memory in Korsakoff Syndrome: Disentangling the Mechanisms of Temporal Confusion Melanie Brion, Philippe de Timary, Anne-Lise Pitel, and Pierre Maurage Background: Korsakoff syndrome (KS), most frequently resulting from alcohol dependence (ALC), is characterized by severe anterograde amnesia. It has been suggested that these deficits may extend to other memory components, and notably source memory deficits involved in the disorientation and temporal confusion frequently observed in KS. However, the extent of this source memory impairment in KS and its usefulness for the differential diagnosis between ALC and KS remain unexplored. Methods: Nineteen patients with KS were compared with 19 alcohol-dependent individuals and 19 controls in a source memory test exploring temporal context confusions (“continuous recognition task”). Episodic memory and psychopathological comorbidities were controlled for. Results: While no source memory deficit was observed in ALC, KS was associated with a significant presence of temporal context confusion, even when the influence of comorbidities was taken into account. This source memory impairment did not appear to be related to performances on episodic memory or executive functions. Conclusions: Patients with KS displayed source memory deficits, as indexed by temporal context confusions. The absence of a relationship with episodic memory performances seems to indicate that source memory impairment is not a mere by-product of amnesia. As ALC was associated with pre- served source memory, the presence of temporal context confusion may serve as a complementary tool for the differential diagnosis between ALC and KS. Key Words: Source Memory, Korsakoff Syndrome, Executive Functions, Alcohol Dependence, Temporal Confusion, Disorientation. K ORSAKOFF SYNDROME (KS), most frequently arising from a combination of alcohol dependence (ALC and thiamine deficiency (Oscar-Berman, 2012), is asso- ciated with several cognitive impairments, notably affecting memory, attentional, and executive abilities (Maharasingam et al., 2013; Pitel et al., 2014). However, the core neuropsy- chological deficit in KS concerns episodic memory, with moderate retrograde but severe anterograde amnesia (But- ters and Brandt, 1985; Talland, 1965). Beyond episodic mem- ory, KS might also significantly impair other memory functions, and notably source memory (Kessels et al., 2008), which constitutes a critical memory system as it allows gathering contextual details related to specific events and retrieving the temporal order of stored information (El Haj et al., 2015). It relies on 2 distinct components: source moni- toring (i.e., identifying and attributing the contextual origin of encoded memories) and reality filtering [i.e., discriminat- ing externally (e.g., real events) and internally (e.g., thoughts) generated information (Johnson et al., 1993)]. Source mem- ory deficits, namely the inability to remember contextual and temporal information about encoded memories, have been identified in various neurological disorders (El Haj et al., 2012; Schwartz et al., 2002). It has moreover been suggested that they play a role, together with impaired strategic search (related to frontal lobe dysfunctions) and impaired episodic memory (Moscovitch and Melo, 1997), in temporal disorien- tation and spontaneous confabulations (Bouzerda-Wahlen et al., 2013; Johnson et al., 1993; Schnider et al., 1996a). Memory distortions and disorientation have been reported since the seminal description of KS (Korsakoff, 1889) and are still frequently described in this population. Therefore, offering a better understanding of the deficits related to the temporal component of source memory in KS might help to disentangle the mechanisms underlying temporal confusions and disorientation. However, very little is currently known regarding specific source memory deficits in KS. The macrostructural brain profile classically observed in KS combines frontal and sub- cortical shrinkage centrally involving fronto-cerebellar and From the Laboratory for Experimental Psychopathology (MB, PT, PM), Psychological Sciences Research Institute, Universite catholique de Louvain, Louvain-la-Neuve, Belgium; Department of Adult Psychiatry (PT), St Luc Hospital and Institute of Neuroscience, Universite catholi- que de Louvain, Brussels, Belgium; and INSERM (A-LP), Ecole Pra- tique des Hautes Etudes, Universite de Caen-Basse Normandie, Unite U1077, GIP Cyceron, CHU Caen, Caen, France. Received for publication September 5, 2016; accepted December 17, 2016. Reprint requests: Pierre Maurage, Universite catholique de Louvain, Institut de Psychologie, LEP, Place du Cardinal Mercier, 10, B-1348 Louvain-la-Neuve, Belgium; Tel.: +32-10-479245; Fax: +32-10- 473774; E-mail: pierre.maurage@uclouvain.be Copyright © 2017 by the Research Society on Alcoholism. DOI: 10.1111/acer.13318 596 Alcohol Clin Exp Res, Vol 41, No 3, 2017: pp 596–607 ALCOHOLISM:CLINICAL AND EXPERIMENTAL RESEARCH Vol. 41, No. 3 March 2017