Contribution of Thalamocortical Loops to the Development, Persistence, and Complications of Alcohol Use Disorder

Abstract

Abstract Alcohol use disorder (AUD) is associated with episodic memory impairments, executive dysfunction, and craving. These cognitive and behavioral alterations are related to brain abnormalities in 3 thalamocortical loops involving different thalamic nuclei. First, when AUD is combined with thiamine deficiency, the anterior nuclei are especially affected, leading to severe dysfunction within the Papez circuit and to the development of Korsakoff’s syndrome (KS). Although episodic memory disorders occur in AUD patients without KS, the specific relationships between the anterior nuclei integrity and episodic memory performance have received little attention in AUD and KS patients. Second, chronic and excessive alcohol consumption also results in dysfunction of the frontocerebellar circuit that theoretically includes the mediodorsal nuclei. Altered executive abilities and motor disorders associated with this system can thus be observed both in AUD patients with and without KS. In AUD, these executive deficits contribute to the persistence of drinking behaviors, hamper psychosocial treatment, and favor relapse. Third, craving, the irrepressible urge to consume a substance or engage in an activity, is now a central feature of AUD and is hypothesized to be subserved by a thalamo-insular circuit involving the ventromedial nuclei of the thalamus. Alterations to several thalamocortical loops thus contribute to the development, persistence, and complications of AUD. The literature reviewed shows a clear involvement of different thalamic nuclei in components of AUD functional sequelae.