Abstract
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.
Highlights
Alcohol use disorder (AUD), a problematic pattern of alcohol use accompanied by clinically significant impairment or distress (American Psychiatric Association, 2013), is one of the leading causes of morbidity and mortality worldwide (GBD 2016 Alcohol Collaborators, 2018)
After identifying compulsivity as a promising and neglected target domain for new treatment approaches in AUD, we discuss neuromodulatory interventions in order to improve recovery in AUD. Such as AUD, whose development relies on learning, rTMS gives the unique opportunity to non-invasively act on target neurocircuits with the best space-time resolution
It guides the implementation of a stepped care approach, that considers different diagnostic and treatment strategies in relation to the stages of AUD, underlying the importance of assessing and treating compulsivity. It supports recovery as a realistic goal, based on the opportunity of modulating neuroplasticity. It supports the implementation of studies aimed to investigate neuromodulation as a promising treatment strategy
Summary
Alcohol use disorder (AUD), a problematic pattern of alcohol use accompanied by clinically significant impairment or distress (American Psychiatric Association, 2013), is one of the leading causes of morbidity and mortality worldwide (GBD 2016 Alcohol Collaborators, 2018). Interactions between the dorsolateral prefrontal (DLPFC), inferior parietal lobule (IPL), orbital frontal cortex (FOC), amygdala and brainstem centers such as the locus coeruleus or the ventral tegmental area, enable the ACC to integrate sensitive information in real time to monitor conflict of competitive cognitive tasks, modulate cognitive control and produce balanced behavior (Yeterian and Pandya, 1985; Cohen et al, 2000) It appears that alterations in the ACC and its associated frontostriatal network (primarily the caudate nucleus and putamen being its subcortical counterpart), which are driving executive function, are critical in executive dysfunction.
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