Neuromodulatory Treatments for Alcohol Use Disorder: A Review

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Abstract

Alcohol use disorder (AUD) is a prevalent condition characterized by chronic alcohol-seeking behaviors and has become a significant economic burden with global ramifications on public health. While numerous treatment options are available for AUD, many are unable to sustain long-term sobriety. The nucleus accumbens (NAcc) upholds an integral role in mediating reward behavior and has been implicated as a potential target for deep brain stimulation (DBS) in the context of AUD. DBS is empirically thought to disrupt pathological neuronal synchrony, a hallmark of binge behavior. Pre-clinical animal models and pilot human clinical studies utilizing DBS for the treatment of AUD have shown promise for reducing alcohol-related cravings and prolonging abstinence. In this review, we outline the various interventions available for AUD, and the translational potential DBS has to modulate functionality of the NAcc as a treatment for AUD.

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The neural basis of drug craving: an incentive-sensitization theory of addiction.

T E Robinson, K C Berridge (1993)

This paper presents a biopsychological theory of drug addiction, the 'Incentive-Sensitization Theory'. The theory addresses three fundamental questions. The first is: why do addicts crave drugs? That is, what is the psychological and neurobiological basis of drug craving? The second is: why does drug craving persist even after long periods of abstinence? The third is whether 'wanting' drugs (drug craving) is attributable to 'liking' drugs (to the subjective pleasurable effects of drugs)? The theory posits the following. (1) Addictive drugs share the ability to enhance mesotelencephalic dopamine neurotransmission. (2) One psychological function of this neural system is to attribute 'incentive salience' to the perception and mental representation of events associated with activation of the system. Incentive salience is a psychological process that transforms the perception of stimuli, imbuing them with salience, making them attractive, 'wanted', incentive stimuli. (3) In some individuals the repeated use of addictive drugs produces incremental neuroadaptations in this neural system, rendering it increasingly and perhaps permanently, hypersensitive ('sensitized') to drugs and drug-associated stimuli. The sensitization of dopamine systems is gated by associative learning, which causes excessive incentive salience to be attributed to the act of drug taking and to stimuli associated with drug taking. It is specifically the sensitization of incentive salience, therefore, that transforms ordinary 'wanting' into excessive drug craving. (4) It is further proposed that sensitization of the neural systems responsible for incentive salience ('for wanting') can occur independently of changes in neural systems that mediate the subjective pleasurable effects of drugs (drug 'liking') and of neural systems that mediate withdrawal. Thus, sensitization of incentive salience can produce addictive behavior (compulsive drug seeking and drug taking) even if the expectation of drug pleasure or the aversive properties of withdrawal are diminished and even in the face of strong disincentives, including the loss of reputation, job, home and family. We review evidence for this view of addiction and discuss its implications for understanding the psychology and neurobiology of addiction.

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Deep brain stimulation of the nucleus accumbens for treatment-refractory obsessive-compulsive disorder.

Damiaan Denys, Mariska Mantione, Martijn Figee … (2010)

Obsessive-compulsive disorder (OCD) is a chronic psychiatric disorder that affects 2% of the general population. Even when the best available treatments are applied, approximately 10% of patients remain severely afflicted and run a long-term deteriorating course of OCD. To determine whether bilateral deep brain stimulation of the nucleus accumbens is an effective and safe treatment for treatment-refractory OCD. The study consisted of an open 8-month treatment phase, followed by a double-blind crossover phase with randomly assigned 2-week periods of active or sham stimulation, ending with an open 12-month maintenance phase. Academic research. Patients Sixteen patients (age range, 18-65 years) with OCD according to DSM-IV criteria meeting stringent criteria for refractoriness to treatment were included in the study. Treatment with bilateral deep brain stimulation of the nucleus accumbens. Primary efficacy was assessed by score change from baseline on the Yale-Brown Obsessive Compulsive Scale (Y-BOCS). Responders were defined by a score decrease of at least 35% on the Y-BOCS. In the open phase, the mean (SD) Y-BOCS score decreased by 46%, from 33.7 (3.6) at baseline to 18.0 (11.4) after 8 months (P < .001). Nine of 16 patients were responders, with a mean (SD) Y-BOCS score decrease of 23.7 (7.0), or 72%. In the double-blind, sham-controlled phase (n = 14), the mean (SD) Y-BOCS score difference between active and sham stimulation was 8.3 (2.3), or 25% (P = .004). Depression and anxiety decreased significantly. Except for mild forgetfulness and word-finding problems, no permanent adverse events were reported. Bilateral deep brain stimulation of the nucleus accumbens may be an effective and safe treatment for treatment-refractory OCD. isrctn.org Identifier: ISRCTN23255677.

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Journal ID (nlm-ta): Brain Sci

Journal ID (iso-abbrev): Brain Sci

Journal ID (publisher-id): brainsci

Title: Brain Sciences

Publisher: MDPI

ISSN (Electronic): 2076-3425

Publication date (Electronic): 28 May 2018

Publication date Collection: June 2018

Volume: 8

Issue: 6

Electronic Location Identifier: 95

Affiliations

Department of Neurosurgery, Stanford University School of Medicine, 300 Pasteur Drive, Edwards Bldg./R-227, Stanford, CA 94305, USA; asalib.ucsandiego@ 123456gmail.com (A.-M.N.S.); allenlho@ 123456gmail.com (A.L.H.); esussman@ 123456stanford.edu (E.S.S.); apendhar@ 123456stanford.edu (A.V.P.)

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[* ]Correspondence: chalpern@ 123456stanford.edu ; Tel.: +1-(650)-723-5574; Fax: +1-(650)-725-8279

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Publisher ID: brainsci-08-00095

DOI: 10.3390/brainsci8060095

PMC ID: 6025548

PubMed ID: 29843426

SO-VID: a93b1f86-5531-4f6f-b519-c3d9c26e90b5

License:

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

Neuromodulatory Treatments for Alcohol Use Disorder: A Review

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Karger: Neurology and Neuroscience

Most cited references 58

The neural basis of drug craving: an incentive-sensitization theory of addiction.

Matching Alcoholism Treatments to Client Heterogeneity: Project MATCH posttreatment drinking outcomes.

Deep brain stimulation of the nucleus accumbens for treatment-refractory obsessive-compulsive disorder.

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