EXPLORING COMORBID OBSESSIVE-COMPULSIVE DISORDER AND ALCOHOL USE DISORDER USING NEUROPSYCHOLOGICAL TOOLS: A PRELIMINARY ANALYSIS

EXPLORING COMORBID OBSESSIVE-COMPULSIVE DISORDER AND ALCOHOL USE DISORDER USING NEUROPSYCHOLOGICAL TOOLS: A PRELIMINARY ANALYSIS

Abstracts an operant observing response task with uncertain reinforcement: A novel possible model of OCD. Behavioural Brain Research 264, 207–229. htt...

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Abstracts an operant observing response task with uncertain reinforcement: A novel possible model of OCD. Behavioural Brain Research 264, 207–229. http://dx.doi.org/10.1016/j.euroneuro.2015.06.030

OBSESSIVE-COMPULSIVE DISORDER CLINICAL STAGING: FROM ENDOPHENOTYPE TO BEHAVIORAL ADDICTION (A THEORETICAL FRAMEWORK)

Giacomo Grassi

897 alarm stage. In this stage the patient has the OCD onset and the anxiety dimension is prominent. Third stage: the reward dysfunction stage. In this stage the patient becomes addicted to compulsions. In our model the OCD patient become addicted to compulsions through the same stages of addiction. Compulions are effective in reducing anxiety in the first stages (binge stage) and become progressively just a habit during the tolerance and withdrawal/habit stages Conclusions: Defining and testing a clinical staging model for OCD could be relevant both in the definition of its pathophisiology and in developing new strategies for an earlier intervention.

University of Florence, Neuroscience, Florence, Italy

Financial disclosure Purpose of the study: Up to date, no clinical staging models have been proposed or tested for obsessive-compulsive disorder (OCD). The last years’ research has clearly recognized the phenotypical and neurobiological heterogeneity of OCD and has focus on sub-typing OCD both in terms of symptom dimensions and comorbidity patterns. However, there are several evidences supporting the idea that the illness course is responsible for neurobiological changes. Consequently, is reasonable to suppose that these neurobiological changes could be responsible for changes in the phenotypical and clinical expression of the disease (de Wit et al., 2014). Moreover, longitudinal studies showed that longer duration of illness is a significant predictor of poor long-term course, highlighting the critical importance of early detection and treatment of OCD. Thus, defining and testing a clinical staging model for OCD could be relevant both in the definition of its pathophisiology and in developing new strategies for an earlier intervention. Methods: Here, we propose a theoretical staging model based on a putative course of the foundamental neurophenomenological dimensions of OCD and we describe the progressive shift from an anxiety disorder to a behavioral addiction during the course of illness. Results: Reward dysfunction represents a key feature of addiction progression. Although anxiety symptoms are a core feature of OCD, current literature shows growing evidences of a reward dysfunction in OCD, mainly in resistant patients. These data support the hypothesis that addiction and OCD share some common neurobiological dysfunctions and have led some authors to view OCD as a behavioural addiction. In this perspective patients may develop a dependency upon compulsive behaviours, because of their rewarding effect when performed perfectly or when compulsions reduce obsessioninduced anxiety and distress (Figee et al., 2011). The corticostriatal loop is clearly involved in OCD pathophysiology and neurophenomenology (Menzies et al., 2003). In this loop we can identify three main neurophenomenological dimensions of OCD: the cognitive dimension (motor disinhibition and cognitive inflexibility), the anxiety dimension and the reward dysfunction dimension. In a clinical staging perspective these dimensions appear at different time during the course of illness in a three stage model representing the progressive shift from frontoamygdalar dysfunction to nucleus accumbens dysfunction. First stage: the endophenotype stage. In this stage the patient present only subtreshold symptoms, but show endophenotypical abnormalities such as motor disinhibition and cognitive inflexibility. Second stage: the anxiety/

The authors did not receive any financial support for this study

References de Wit, SJ, Alonso, P, Schweren, L, Mataix-Cols, D, Lochner, C, Menchón, JM, Stein, DJ, Fouche, JP, Soriano-Mas, C, Sato, JR, Hoexter, MQ, Denys, D, Nakamae, T, Nishida, S, Kwon, JS, Jang, JH, Busatto, GF, Cardoner, N, Cath, DC, Fukui, K, Jung, WH, Kim, SN, Miguel, EC, Narumoto, J, Phillips, ML, Pujol, J, Remijnse, PL, Sakai, Y, Shin, NY, Yamada, K, Veltman, DJ, van den Heuvel, OA., 2014. Multicenter voxel-based morphometry mega-analysis of structural brain scans in obsessivecompulsive disorder. Am J Psychiatry 1 171 (3), 340–349. Figee, M, Vink, M, de Geus, F, Vulink, N, Veltman, DJ, Westenberg, H, Denys, D., 2011. Dysfunctional reward circuitry in obsessivecompulsive disorder. Biol Psychiatry 69 (9), 867–874. Menzies, L, Chamberlain, SR, Laird, AR, Thelen, SM, et al., 2008. Integrating evidence from neuroimaging and neuropsychological studies of obsessive-compulsive disorder: the orbitofronto-striatal model revisited. Neuroscience and Biobehavioral Reviews 32, 525–549. http://dx.doi.org/10.1016/j.euroneuro.2015.06.031

EXPLORING COMORBID OBSESSIVE-COMPULSIVE DISORDER AND ALCOHOL USE DISORDER USING NEUROPSYCHOLOGICAL TOOLS: A PRELIMINARY ANALYSIS

Olga Angera,b, Natalie L. Cuzenc, Yana Varlakovaa,b, Grace A. Daya,b, Claire C. Gilland, Dan Steinc, Keith Lawsb, Naomi A. Fineberga,b a

National Obsessive Compulsive Disorders Specialist Service, Hertfordshire Partnership NHS University Foundation Trust, United Kingdom. bUniversity of Hertfordshire, United Kingdom. cUniversity of Cape Town, South Africa. dUniversity of Cambridge, BCNI, United Kingdom By investigating neuropsychological profiles in patients with obsessive-compulsive disorder (OCD) and OCD with alcohol use disorder (OCD þAUD), focusing on tasks of behavioural inhibition, attentional set-shifting and decision-making, we

898 aimed to elucidate factors contributing to compulsive behaviour. Consenting patients (n ¼24) were recruited from outpatient clinics and attributed to DSM-IV OCD (n ¼14) or OCDþ AUD (n ¼10) groups. Healthy controls with no relevant family history (n¼ 15) were identified through established databases and public advertisement. We used the Barratt Impulsiveness Scale (BIS) to assess behavioural impulsivity, the Stop-Signal Task for motor response inhibition, the Intradimensional-Extradimensional (ID-ED) SetShift Task for attentional flexibility and the Cambridge Gamble Task (CGT) for decision-making. Analysis of covariance was used to test for group differences, controlling for depression (Montgomery-Asberg Depression Rating Scale) and anxiety (State-Trait Anxiety Inventory), for which both patient groups scored significantly higher (po.003) than controls. We additionally controlled for pre-morbid intelligence estimated by the National Adult Reading Test (NART). When we co-varied for anxiety and depression, both patient groups showed poorer attentional flexibility on the ID-ED task than controls (p¼.01, with large effect size). Motor response inhibition (SST) did not differ between groups, however the OCDþAUD group showed poorer attentional inhibition than both other groups on the attentional subscale of BIS (p¼.001). The quality of CGT decision-making was also significantly poorer in the OCDþAUD group than in the pure OCD group and controls (p¼ .05). Interestingly, significantly higher (po.001) NART errors were observed in the OCDþAUD group (M¼ 16, SE¼ 2.3) compared with the pure OCD group (M¼ 10.3, SE¼ .9) and controls (M¼ 7.8, SE¼ 1). When we additionally co-varied for intelligence, the previously significant results were no longer observed. Although our interpretations are limited by small sample size, it appears the impairment in decision-making, setshifting and attentional impulsivity observed in OCDþAUD may be attributable to between-group differences in intelligence. There is some evidence that lower premorbid IQ may be linked with AUD, specifically in those patients with a strong family history of AUD. On the other hand, questions have been raised as to the validity of the NART as a specific measure of premorbid IQ in AUD. Future such studies should pay close attention to measuring to premorbid intelligence and its relationship with neurocognitive performance.

H. Nicolini et al. Background: Hoarding disorder has been estimated to affect 2–5% of adults during their lifetime. It is a chronic condition which tends to manifest as a clinical problem later in life, yet it has been established that certain characteristics could begin in early adulthood. It is defined as acquisition and failure to discard objects of little value or use. This results in heavily cluttered living spaces, making them unusable. This condition is very disabling and accidental fatalities have occurred due to unsafe accumulations of objects. Although there are instruments which measure the severity of Hoarding Disorder, there is a lack of a simpleself-administered screening questionnaire for the condition. This study therefore chose to conduct preliminary validation on the HOARD Questionnaire, which is a five-item, binary response, screening questionnaire for Hoarding Disorder. It has been developed at the National and Trustwide OCD/BDD Service, South West London and St. George's Mental Health NHS Trust. Methods: Patients treated by the National and Trustwide Service for OCD/BDD, were asked to complete the HOARD questionnaire. All patients’ responses were compared with their diagnosis of Hoarding Disorder which was made following observation and interviews in their home by specialist mental health workers. Results: Fifty-two patients completed the questionnaire, five of whom, had significant Hoarding Disorder on clinical assessment. Using a score of 3/5, the HOARD identified three of these five patients (false positive result in 13/52) (sensitivity 60.0% and specificity 72.3%). Conclusions: Further investigation with a larger number of subjects is necessary before the use of the HOARD can be advocated widely. This preliminary investigation suggests it is an easy to use, sensitive and specific tool, which may have a future role in early identification of individuals at a risk of developing Hoarding Disorder. http://dx.doi.org/10.1016/j.euroneuro.2015.06.033

CITALOPRAM PULSE-LOADING FOR TREATMENT-RESITANT OBSESSIVE-COMPULSIVE DISORDER: PRELIMINARY DATA FROM AN OPEN-LABEL TRIAL

Giacomo Grassi, Stefano Pallanti http://dx.doi.org/10.1016/j.euroneuro.2015.06.032

THE DEVELOPMENT OF THE HOARD QUESTIONNAIRE: A SCREENING INSTRUMENT FOR HOARDING DISORDER.

C.L. English ((medical student)), H Tyagi ((Research Registrar)), L.M. Drummond ((Consultant Psychiatrist and Senior Lecturer)) SW London and St George's Mental Health NHS Trust and St George's, University of London Aims and hypothesis: The aim of this study was to conduct preliminary validation of a self-administered five ítem screening questionnaire for Hoarding Disorder.

University of Florence, Neurofarba, Florence, Italy Purpose of the study: Treatment resistance is a frequent situation in Obsessive Compulsive Disorder (OCD), occurring in 40–60% of patients. However, in the current literature there are only a few evidence-based options for treatment resistant patients. Pulse-loading treatment consists in a rapid titration of the pharmacological agent in the first days of treatment. A few studies suggested that this kind of titration with intravenous clomipramine could result in a greater and faster response than with a standard titration in OCD resistant patients (Koran et al., 2006; Grassi et al., 2013). The aim of this open-label trial was to investigate the effectiveness and tolerability of a citalopram pulse-loading protocol in severe treatment-resistant OCD patients. Methods: We enrolled 7 severe treatment-resistant OCD patients. Treatment-resistance was defined as non-response