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5 How to integrate the neuropsychological assessment as key information for relevant clinical decisions in AUD treatment? Early after the cessation of alcohol drinking, a neuropsychological assessment enables clinicians to offer AUD patients the best treatment options according to their neuropsychological profile. When neuropsychological abilities are preserved, patients can benefit from usual treatment. When patients exhibit mild-tomoderate neuropsychological deficits, they can be referred to midterm care units to permit spontaneous cognitive recovery without drinking potentially favored by neuropsychological rehabilitation. After several weeks, they can be reevaluated: a significant neuropsychological recovery would allow attending usual treatment, while persisting neuropsychological deficits would require specialized care, just as patients with severe neuropsychological deficits, including neuropsychological rehabilitation programs.

5 How to integrate the neuropsychological assessment as key information for relevant clinical decisions in AUD treatment? Early after the cessation of alcohol drinking, a neuropsychological assessment enables clinicians to offer AUD patients the best treatment options according to their neuropsychological profile. When neuropsychological abilities are preserved, patients can benefit from usual treatment. When patients exhibit mild-tomoderate neuropsychological deficits, they can be referred to midterm care units to permit spontaneous cognitive recovery without drinking potentially favored by neuropsychological rehabilitation. After several weeks, they can be reevaluated: a significant neuropsychological recovery would allow attending usual treatment, while persisting neuropsychological deficits would require specialized care, just as patients with severe neuropsychological deficits, including neuropsychological rehabilitation programs.

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... Executive functioning deficits in AUD are pronounced and pose liability for continued use and relapse [101,102,103,104]. Of these EF deficits, behavioral control (impulsivity), Content courtesy of Springer Nature, terms of use apply. ...
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Purpose of review This article utilizes a pre-existing framework in the field of addiction to comprehensively capture the effects of classic psychedelics (psilocybin, lysergic acid diethylamide, dimethyltryptamine, and mescaline) for the treatment of alcohol use disorder (AUD). Recent findings Basic science, preclinical, and clinical studies support the influence of psychedelics on all 3 core domains of addiction, comprising negative emotionality (including depression and anxiety), incentive salience (including craving and compulsive use) and executive functioning (including impulsivity and cognitive flexibility). However, systematic investigation using objective measures to evaluate these domains in AUD is needed. Summary We close by discussing limitations and challenges in the field of psychedelic science, and propose future research directions to advance our understanding of the psychological and neurobiological basis of clinical improvement. Conceptualizing future research under this 3-domain framework may assist the refinement of psychedelic-assisted treatments and the development of personalized medicine approaches for AUD.
... Follow-Back, 160 Indeed, one phase-I study of 5-MeO-DMT that used individualized dosing regimens (2, 6, 12, and 18 mg) seems to support this. 82 179,180 Notably, several authors posit that abstinence of alcohol leads to (partial) recovery of neuropsychological functioning. 181,182 Yet, others argue that impairments persist even after sobriety. ...
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... In addition, alcohol-related neuropsychological impairments have been widely described in the literature, being executive functions, with working and episodic memory frequently affected [42]. Many experimental paradigms have been used to evaluate the memory deficits in alcohol-treated rats. ...
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... Alcohol-related neuropsychological impairments have been widely described in the literature, being executive functions, working and episodic memory frequently affected [48]. Many experimental paradigms have been used to evaluate memory deficits in alcohol-treated rats. ...
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Wernicke-Korsakoff syndrome (WKS) is induced by thiamine deficiency (TD) and mainly related to alcohol consumption. Frontal cortex dysfunction has been associated to impulsivity and disinhibition in WKS patients. The pathophysiology involves oxidative stress, excitotoxicity and inflammatory responses leading to neuronal death, but the relative contributions of each factor (alcohol and TD, isolate or in interaction) to these phenomena are still poorly understood. A rat model was used by forced consumption of 20% (w/v) alcohol for 9 months (CA), TD hit (TD diet + pyrithiamine 0.25 mg/kg, i.p. daily injections the last 12 days of experimentation; TDD), and both combined treatments (CA+TDD). Motor and cognitive performance and cortical damage were examined. CA caused hyperlocomotion as a possible sensitization of ethanol-induced excitatory effects and recognition memory deficits. In addition, CA+TDD animals showed a disinhibited-like behavior, which appears to be dependent on TDD. Also, combined treatment led to more pronounced alterations in nitrosative stress, lipid peroxidation, apoptosis and cell damage markers. Correlations between injury signals and disinhibition suggest that CA+TDD disrupts behaviors dependent on the frontal cortex. Our study sheds light on the potential disease-specific mechanisms, reinforcing the need for neuroprotective therapeutic approaches along with preventive treatments for the nutritional deficiency in WKS.
... A LCOHOL-RELATED NEUROPSYCHOLOGICAL IMPAIRMENTS have been widely described in the literature. Executive functions, working memory, episodic memory, visuospatial, and motor abilities are, among others, indeed frequently affected by chronic and excessive alcohol consumption (Maillard et al., 2020;Oscar-Berman et al., 2014, for a review). The neuropsychological assessment of patients with alcohol use disorder (AUD) is crucial early after detoxification. ...
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Alcohol use disorder (AUD) is a chronic relapsing disorder, which enforces a person to compulsively seek alcohol, restricting control over alcohol intake leads to emergence of an undesired emotional state during abstinence. There are recent advances for better understanding of neurocircuitry involved in the pathophysiology of AUD. Alcohol interaction with neuronal membrane proteins results in changes in neuronal circuits. It is also linked with the potential medication and their clinical validation concerning their pharmacological targets for alcoholic abstinence. This review covers research work from the past few decades on the therapeutic advances on treatment of alcohol dependence; further detailing the fundamental neurochemical mechanisms after alcohol administration. It also covers interaction of alcohol with GABAergic, glutaminergic, dopaminergic, serotonergic and opioid systems. This review further elaborated the neurobiology of noradrenergic, cholinergic and cannabinoid systems and their interaction with AUD. Elaborative information of potential drug targets under current exploration for AUD treatment with their mechanisms are reported here along with clinical outcomes and the associated side effects. Graphic Abstract Open image in new window