Despite longitudinal studies reporting symptomatic remission rates ranging from 32% to 70%, Obsessive-Compulsive Disorder is considered a persistent and very disabling disorder. However, these studies suggest that recovery can be a realistic goal for a subgroup of the Obsessive-Compulsive Disorder population and that a clear definition of recovery is timely in Obsessive-Compulsive Disorder. The aim of this paper is to discuss the dimensions of and propose an operational definition of recovery in Obsessive-Compulsive Disorder. Considering the impact generated by the definition of recovery for other mental disorders, this article discusses how this concept may shape the future of research and clinical practice in Obsessive-Compulsive Disorder. Ultimately, the hope is that the management of Obsessive-Compulsive Disorder may parallel, and expand upon, some of the current approaches implemented in the care of schizophrenia, so that early diagnosis, stepped-care techniques, and a personalized approach can be used to create recovery-oriented treatment programs and influence policy making for Obsessive-Compulsive Disorder.

There is evidence that EO might be considered the neurodevelopmental subtype of OCD. Indeed there is evidence that different clusters of symptoms and dimensions at an early stage predict different trajectories in phenotype and that distinct neurocircuit patwhays underpin the progression of the disorder. Despite the development of high refractoriness in the course of the disorder, evidence suggests that EO may be particularly treatment responsive in the early stages, thus showing the need for early recognition and additional recovery oriented studies in this subgroup. Consistent with the neurodevelopmental perspective, immunity and glutamate neurotransmission are emerging as novel pathways for parsing out the neurobiology of OCD, the EO form in particular, supporting the implementation of new multisystemic models of the OCD phenotype. Brain connectivity patterns, immune and microbiome profiles are standing out as promising areas for biomarkers with the potential for targeted personalized therapies in EO.

Alcohol use Disorder (AUD) is one of the leading causes of morbidity and mortality worldwide. The progression of the disorder is associated with the development of compulsive alcohol use, which in turn contributes to the high relapse rate and poor longer term functioning reported in most patients, even with treatment. While the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) defines AUD by a cluster of symptoms, parsing its heterogeneous phenotype by domains of behavior such as compulsivity may be a critical step to improve outcomes of this condition. Still, neurobiological underpinnings of compulsivity need to be fully elucidated in AUD in order to better design targeted treatment strategies. In this manuscript, we review and discuss findings supporting common mechanisms between AUD and OCD, dissecting the construct of compulsivity and focusing specifically on characteristic disruptions in habit learning and cognitive control in the two disorders. Finally, neuromodulatory interventions are proposed as a probe to test compulsivity as key pathophysiologic feature of AUD, and as a potential therapy for the subgroup of individuals with compulsive alcohol use, i.e., the more resistant stage of the disorder. This transdiagnostic approach may help to destigmatize the disorder, and suggest potential treatment targets across different conditions.