The Nature of Facial Expression Recognition Deficits Following Orbitofrontal Cortex Damage Megan L. Willis Australian Catholic University, Sydney, Australia and Macquarie University Romina Palermo ARC Centre of Excellence in Cognition and Its Disorders, Perth, Australia and University of Western Australia Ky McGrillen Royal Prince Alfred Hospital, Sydney, Australia Laurie Miller ARC Centre of Excellence in Cognition and Its Disorders, Sydney, Australia, and Royal Prince Alfred Hospital, Sydney, Australia, and Central Medical School, University of Sydney Objective: Orbitofrontal cortex (OFC) damage has been associated with facial expression recognition deficits in some, but not all, previous studies. The pattern of performance of a group of patients with OFC damage was assessed across a series of facial expression recognition tasks. We aimed to determine whether some tasks were more sensitive at detecting deficits than others. Method: Seven patients with damage to the OFC, 6 control patients with frontal lesions that spared the OFC, and a group of healthy controls completed a series of facial expression recognition tasks including 2 labeling tasks and 2 matching tasks. Results: The OFC patient group demonstrated impaired labeling of negative facial expressions (i.e., anger, disgust, fear, and sadness) shown for a short time (500 ms) relative to the comparison groups. When facial expressions were shown for a longer time (5,000 ms), the OFC patient group’s performance did not differ significantly from either comparison group. The OFC patient group was impaired when matching subtle, low intensity negative facial expressions, but not when matching high intensity, prototypical facial expressions. Conclusions: The pattern of performance across tasks revealed that only certain facial expression recognition tasks appear to be sufficiently sensitive to detect deficits in patients with OFC damage. These findings have important implications for the assessment of facial expression recognition difficulties in patients with OFC damage and more broadly, for special populations. Keywords: facial expression recognition, emotion, orbitofrontal cortex, prefrontal cortex, frontal lobes Patients who have sustained damage to the orbitofrontal cortex (OFC), a brain region that occupies the ventral surface of the frontal lobes (Kringelbach & Rolls, 2004), often perform normally on standard neuropsychological batteries yet exhibit abnormalities in emotional and social functioning, such as frequently making social faux pas (Zald & Andreotti, 2010). One factor that may be associated with their poor emotional and social functioning is impaired facial expression recognition. Impaired facial expression recognition is typical in other dis- orders involving abnormal social functioning, such as schizo- phrenia and autism spectrum disorders (e.g., Hall et al., 2004; Humphreys, Minshew, Leonard, & Behrmann, 2007). The OFC also is thought to be an important neural region in the facial expression recognition network (Adolphs, 2002). Thus, the extent to which damage to the OFC impairs facial expression recognition has been of particular research interest. However, the evidence is not consistent. Some patient studies have shown that OFC damage is associated with an impaired ability to categorize or rate the intensity of facial expressions (e.g., Blair & Cipolotti, 2000; Dal Monte et al., 2013; Heberlein, Padon, Gillihan, Farah, & Fellows, 2008; Hornak, Rolls, & Wade, 1996; Marinkovic, Trebon, Chauvel, & Halgren, 2000). In these instances where deficits have been observed, they typically reflect difficulty recognizing negative emotions (e.g., sadness, anger) as opposed to positive (e.g., happy) emotions (see Heberlein et al., 2008; Zald & Andreotti, 2010, for reviews). However, a number of other studies have failed to observe any evidence of facial expression recognition deficits in patients who have sustained damage to the OFC (e.g., Adolphs, Damasio, Tranel, Cooper, & Damasio, 2000; Beer, Heerey, Keltner, Scabini, & Knight, 2003; Hornak et al., 2003; Willis, Palermo, Burke, McGrillen, & Miller, 2010). Explaining these conflicting findings has been complicated by the divergent methodologies employed This article was published Online First March 3, 2014. Megan L. Willis, School of Psychology, Australian Catholic University, Sydney, Australia and Department of Cognitive Science, Macquarie Uni- versity, Sydney, Australia; Romina Palermo, ARC Centre of Excellence in Cognition and Its Disorders, Perth, Australia and School of Psychology, University of Western Australia, Perth, Australia; Ky McGrillen, Radiology Department, Royal Prince Alfred Hospital, Sydney, Australia; Laurie Miller, ARC Centre of Excellence in Cognition and Its Disorders, and Neuropsychology Unit, Royal Prince Alfred Hospital, and Central Medical School, University of Sydney, Sydney, Australia. Correspondence concerning this article should be addressed to Megan Willis, School of Psychology, Australian Catholic University, Mount St Mary Campus, 25a Barker Road, Strathfield, NSW, 2135, Australia. E-mail: dr.megan.willis@gmail.com This document is copyrighted by the American Psychological Association or one of its allied publishers. This article is intended solely for the personal use of the individual user and is not to be disseminated broadly. Neuropsychology © 2014 American Psychological Association 2014, Vol. 28, No. 4, 613– 623 0894-4105/14/$12.00 DOI: 10.1037/neu0000059 613