Obsessive-compulsive disorder (OCD) is a common psychiatric condition classically characterized by obsessions (recurrent, intrusive and unwanted thoughts) and compulsions (excessive, repetitive and ritualistic behaviors or mental acts). OCD is heterogeneous in its clinical presentation and not all patients respond to first-line treatments. Several neurocircuit models of OCD have been proposed with the aim of providing a better understanding of the neural and cognitive mechanisms involved in the disorder. These models use advances in neuroscience and findings from neuropsychological and neuroimaging studies to suggest links between clinical profiles that reflect the symptoms and experiences of patients and dysfunctions in specific neurocircuits. Several models propose that treatments for OCD could be improved if directed to specific neurocircuit dysfunctions, thereby restoring efficient neurocognitive function and ameliorating the symptomatology of each associated clinical profile. Yet, there are several important limitations to neurocircuit models of OCD. The purpose of the current review is to highlight some of these limitations, including issues related to the complexity of brain and cognitive function, the clinical presentation and course of OCD, etiological factors, and treatment methods proposed by the models. We also provide suggestions for future research to advance neurocircuit models of OCD and facilitate translation to clinical application.

Objective: Although attentional bias (AB) toward angry faces is well established in patients with anxiety disorders, it is still poorly studied in obsessive-compulsive disorder (OCD). We investigated whether OCD patients present AB toward angry faces, whether AB is related to symptom severity and whether AB scores are associated with specific OCD symptom dimensions. Method: Forty-eight OCD patients were assessed in clinical evaluations, intelligence testing and a dot-probe AB paradigm that used neutral and angry faces as stimuli. Analyses were performed with a one-sample t-test, Pearson correlations and linear regression. Results: No evidence of AB was observed in OCD patients, nor was there any association between AB and symptom severity or dimension. Psychiatric comorbidity did not affect our results. Conclusion: In accordance with previous studies, we were unable to detect AB in OCD patients. To investigate whether OCD patients have different brain activation patterns from anxiety disorder patients, future studies using a transdiagnostic approach should evaluate AB in OCD and anxiety disorder patients as they perform AB tasks under functional neuroimaging protocols.

OBJETIVO: Recentes estudos utilizando análise fatorial no transtorno obsessivocompulsivo identificaram dimensões consistentes dos sintomas. Este estudo foi delineado para observar quais dimensões dos sintomas obsessivo-compulsivos podem ser modificadas adicionando duas sessões individuais de entrevista motivacional e mapeamento cognitivo à terapia cognitivo-comportamental em grupo usando um ensaio clínico randomizado. MÉTODO: Quarenta pacientes ambulatoriais com diagnóstico primário de transtorno obsessivo-compulsivo foram alocados aleatoriamente para receber terapia cognitivo-comportamental em grupo (grupo controle) ou entrevista motivacional+mapeamento cognitivo+terapia cognitivo-comportamental em grupo. Para avaliar mudanças nas dimensões dos sintomas, foi administrada a Escala Dimensional para Sintomas Obsessivo-Compulsivos de Yale-Brown antes do início e após o tratamento. RESULTADOS: Ao final do tratamento houve diferença estatisticamente significativa entre a terapia cognitivo-comportamental em grupo e entrevista motivacional+mapeamento cognitivo+terapia cognitivocomportamental em grupo na média do escore total da Escala Dimensional para Sintomas Obsessivo-Compulsivos de Yale-Brown e no escore da dimensão de contaminação e agressão. Colecionismo apresentou melhora com tendência estatística. CONCLUSÃO: Esses achados sugerem que acrescentar entrevista motivacional+mapeamento cognitivo à terapia cognitivo-comportamental em grupo pode facilitar mudanças na redução dos escores nas diferentes dimensões dos sintomas, como indicado pela Escala Dimensional para Sintomas Obsessivo-Compulsivos de Yale-Brown. No entanto, são necessários estudos adicionais para confirmar estes resultados.

OBJECTIVE: Recent factor-analytic studies of obsessive-compulsive disorder identified consistent symptom dimensions. This study was designed in order to observe which obsessive compulsive symptom dimensions could be changed by adding two individual sessions of motivational interviewing and thought mapping of cognitive-behavioral group therapy using a randomized clinical trial. METHOD: Forty outpatients with a primary diagnosis of obsessive-compulsive disorder were randomly assigned to receive cognitive-behavioral group therapy (control group) or motivational interviewing+thought mapping plus cognitive-behavioral group therapy. To evaluate changes in symptomdimensions, the Dimensional Yale-Brown Obsessive-Compulsive Scale was administered at baseline and after treatment. RESULTS: At post-treatment, there were statistically significant differences between cognitive-behavioral group therapy and motivational interviewing+thought mapping+cognitivebehavioral group therapy groups in the mean total Dimensional Yale-Brown Obsessive-Compulsive Scale score, and in the contamination and aggression dimension score. Hoarding showed a statistical trend towards improvement. CONCLUSION: These findings suggest that adding motivational interviewing+thought mapping to cognitive-behavioral group therapy can facilitate changes and bring about a decrease in the scores in different obsessive-compulsive disorder symptom dimensions, as measured by the Dimensional Yale-Brown Obsessive-Compulsive Scale. Nonetheless, additional trials are needed to confirm these results.

Despite the fact that majority of OCD patients responds to conventional treatments, about 40% remain symptomatic after appropriate trials with serotonin uptake inhibitors (SRIs) or behavioral therapy. A patient is considered treatment-resistant after failing to respond to three pharmacological trials with SRIs as well as to behavior therapy. When all somatic strategies have been tried, including augmentation with other medications, and the patient remains symptomatic, he or she is considered treatment refractory. The concepts of resistance and refractoriness are briefly revised, and the current augmentation strategies, as well as non-pharmacological approaches such as neurosurgery and transcranial magnetic stimulation, are addressed in this paper. Finally, issues of predictive response factors, pharmacogenetics, and the pathophysiology of resistant cases are suggested as targets for further researches.