Neurocognitive functioning in bulimia nervosa: the role of neuroendocrine, personality and clinical aspects S. Galderisi 1 *, P. Bucci 1 , A. Mucci 1 , L. Bellodi 2 , G. B. Cassano 3 , P. Santonastaso 4 , S. Erzegovesi 2 , A. Favaro 4 , M. Mauri 3 , P. Monteleone 1 and M. Maj 1 1 Department of Psychiatry, University of Naples SUN, Italy 2 Department of Neuropsychiatric Sciences, Vita-Salute University, Istituto Scientifico HS Raffaele, Milan, Italy 3 Department of Psychiatry, Neurobiology, Pharmacology, and Biotechnology, University of Pisa, Italy 4 Department of Neurosciences, University of Padua, Italy Background. Studies investigating neurocognitive impairment in subjects with eating disorders (EDs) have reported heterogeneous patterns of impairment and, in some instances, no dysfunction. The present study aimed to define the pattern of neurocognitive impairment in a large sample of bulimia nervosa (BN) patients and to demonstrate that neuroendocrine, personality and clinical characteristics influence neurocognitive performance in BN. Method. Attention/immediate memory, set shifting, perseveration, conditional and implicit learning were evaluated in 83 untreated female patients with BN and 77 healthy controls (HC). Cortisol and 17b-estradiol plasma levels were assessed. Cloninger’s Temperament and Character Inventory – Revised (TCI-R), the Bulimic Investigation Test Edinburgh (BITE) and the Montgomery–Asberg Depression Rating Scale (MADRS) were administered. Results. No impairment of cognitive performance was found in subjects with BN compared with HC. Cortisol and ‘ Self-directedness ’ were associated with better performance on conditional learning whereas 17b-estradiol had a nega- tive influence on this domain ; ‘ Reward dependence ’ was associated with worse performance on implicit learning ; and depressive symptomatology influenced performance on the Wisconsin Card Sorting Test (WCST) negatively. Conclusions. No cognitive impairment was found in untreated patients with BN. Neuroendocrine, personality and clinical variables do influence neurocognitive functioning and might explain discrepancies in literature findings. Received 17 June 2009 ; Revised 15 May 2010 ; Accepted 20 May 2010 ; First published online 1 July 2010 Key words : Co-morbidity, cognitive functions, eating disorders, neuroendocrine indices, reward dependence. Introduction Cognitive impairment in patients with eating dis- orders (EDs) has been reported by the majority of studies addressing this issue. However, heterogen- eous patterns of cognitive dysfunctions have been found and, in a minority of studies, no dysfunction was observed [see Zakzanis et al. (2010) for a meta- analysis and Appendix 1 (available online) for a de- tailed description of literature data]. The heterogeneity of findings might be due to the use of different neuro- psychological tests, exploring different subdomains of complex cognitive functions. This is particularly true for memory and executive functions, the two most in- vestigated cognitive domains in the literature on EDs. Studies investigating memory dysfunction in EDs have reported either no impairment or deficits in different memory subdomains, such as short-term verbal or visuospatial memory, secondary verbal and/or visuospatial memory and verbal learning (see Appendix 1). In particular, of eight studies exploring memory in patients with bulimia nervosa (BN), three found no impairment, one found impaired short-term and working memory only in subjects with co- morbidity, and four investigated verbal memory and reported impaired learning, secondary memory or short-term memory (see Appendix 1) ; three out of these four also included a test for secondary visuo- spatial memory, but only two reported a deficit in this subdomain. None of the studies carried out in BN patients explored recognition versus free recall to rule out the possibility that the observed memory impair- ment is due to an executive dysfunction, that is a deficit in the ability to initiate a suitable strategy for successful recall. * Address for correspondence : Professor S. Galderisi, Department of Psychiatry, University of Naples SUN, Largo Madonna delle Grazie, 80138 Naples, Italy. (Email : sgalderi@tin.it) Psychological Medicine (2011), 41, 839–848. f Cambridge University Press 2010 doi:10.1017/S0033291710001303 ORIGINAL ARTICLE