Gait ataxia in alcohol use disorder: A systematic review.

OBJECTIVE: A severe and long-term alcohol use can have adverse effects on lower limb function. Over time, some individuals may develop gait ataxia, which refers to the impairment of controlled lower body movements that are important for walking and maintaining proper gait. Gait ataxia is well-documented in patients who have been diagnosed with alcohol-related Wernicke-Korsakoff syndrome (WKS); however, less is known on how common ataxia is among patients with alcohol use disorder (AUD) without WKS. To date, no study has systematically reviewed the evidence focusing on patients suffering only from AUD. Our aim was to perform a qualitative synthesis of the existing literature examining behavioral signs of gait ataxia among abstinent patients with AUD. METHOD: Two facets were created encompassing keywords for "alcohol use disorder" and "measures of gait ataxia." Databases, including EMBASE, APA PsycInfo, Medline, and Cochrane Library, were searched for studies, and a quality assessment was performed. RESULTS: Ten studies were identified (37 ≥ ns ≤ 247), which were all rated as being of moderate (N = 7) to good quality (N = 3). The age range was 31.4-53.4 years (weighted mean age: 53.6 years), and 78.3% of the participants were male. Eight studies found that patients with AUD and without WKS exhibited behavioral signs of gait ataxia. CONCLUSIONS: Although there is evidence of gait ataxia among patients with AUD, heterogeneous results and methodological shortcomings such as lack of screening for neurocognitive deficits deem these findings preliminary and highlight the need for more research in the future. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

The effectiveness of oxytocin for treating substance use disorders:A systematic review of randomized placebo-controlled trials.

Oxytocin is gaining traction in the treatment of various substance use disorders (SUD). We performed a systematic review assessing the efficacy of oxytocin for treating different SUD. The electronic databases MEDLINE, EMBASE, CENTRAL, and the Cochrane Database of Systematic Reviews were searched for randomized controlled trials examining the effects of oxytocin vs. placebo in SUD samples. Quality assessment was conducted using a Cochrane validated checklist. A total of 17 trials with unique samples were identified. These were conducted on participants with SUD involving alcohol (n = 5), opioids (n = 3), opioids and/or cocaine/other stimulants (n = 3), cannabis (n = 2), or nicotine (n = 4). Across the SUD-groups, oxytocin reduced withdrawal symptoms (3/5 trials), negative emotional states (4/11 trials), cravings (4/11 trials), cue-induced cravings (4/7 trials), and consumption (4/8 trials). Sixteen trials had an overall considerable risk of bias. In conclusion, although oxytocin showed some promising therapeutic effects, the findings are too inconsistent and the trials too heterogeneous to derive any firm conclusions. Sounder methodological and well-powered trials are warranted.

Pharmacological treatment of alcohol use disorder in patients with psychotic disorders: A systematic review.

BACKGROUND: Patients with psychotic disorders (PD) often have comorbid alcohol use dis- order (AUD), which is typically treated pharmacologically. Up till now, no systematic review has ex- amined the effectiveness and safety of AUD treatment in PD patients.

Objectives: This study aimed to systematically review the literature on (1) the effects of pharmacolog- ical treatments for AUD on drinking outcomes, (2) the side effects of the drugs, and (3) the effects of polypharmacy in patients with comorbid AUD and PD.

Methods: Bibliographic searches were conducted in MEDLINE, Embase, Cochrane Central Register of Controlled Trials, and PsycINFO. At least two reviewers extracted the data, assessed the risk of bi- as, and performed the qualitative synthesis of the collected evidence.

Results: Twelve eligible studies were identified, half being randomized controlled trials (RCTs). Three studies examined disulfiram, nine naltrexone, two acamprosate, and one nalmefene by comparing the effects of treatment to placebo, baseline, or other pharmacological agents. Disulfiram and naltrexone were shown to reduce alcohol intake. Regarding acamprosate, the findings were mixed. Nalmefene decreased alcohol intake. All pharmacological agents appeared safe to use as AUD mono- therapy, but cardiac events were reported when combining naltrexone and disulfiram. Nine studies had a high risk of bias, and three had some other concerns.

Conclusion: The studies provide tentative support for the use of naltrexone and disulfiram in this population, although combinations of pharmacological AUD treatments and other polypharmacy remain unexplored. The studies had high adherence rates that are hardly replicable in real-world settings.

Comparison of self-reported alcohol consumption and ethyl glucuronide in hair in a sample of 60+ year -olds treated for DSM-5 alcohol use disorder.

There is a lack of evidence for the consistency between self-reported alcohol consumption (SRAC) and concentrations of ethyl glucuronide in hair (hEtG) among elderly patients treated exclusively for alcohol use disorder (AUD). Hence, this study assessed the consistency between these two measures in these patients. A total of 190 patients with AUD were assessed for SRAC using Form 90 and hEtG, 14 or 22 weeks after treatment conclusion. Patients were grouped according to SRAC (g/day) and corresponding hEtG concentrations (pg/mg): 0 and <5 (abstinence), 0.1-14.3 and 5.0-9.9 (low consumption), 14.4-21.4 and 10.0-15.9 (moderate consumption), 21.5-59.9 and 16.0-30 (high consumption) and ≥60 and >30 (excessive consumption). The extent of underreporting and overreporting was examined by crosstabulations, and inter-rater reliability was reported by kappa correlations. Associations and effect modification were examined by conditional logistic regression. Due to multitesting, p-values ≤0.01 were considered significant. Underreporting was found in 96 patients (50.5%) and overreporting in 41 patients (21.6%). The kappa coefficients varied between 0.19 and 0.34. HEtG was more likely to detect low, moderate and high alcohol consumption compared with SRAC (ORs between 5.1 and 12.6, all p-values <0.01), but SRAC and hEtG did not differ significantly with respect to identification of abstinence (OR = 1.9, p = 0.05). Inconsistency between the outcome measures was found in a considerable number of the patients. More studies examining the consistency between SRAC and specific direct biomarkers of alcohol in this population seem warranted.

Relapse prevention for alcohol use disorders: combined acamprosate and cue exposure therapy as aftercare.

AIMS: Many patients with alcohol use disorders are challenged by cravings leading to repeated relapses. Both cue exposure therapy (CET) and acamprosate target alcohol cravings and are often combined (CET + acamprosate). The main aim of this study was to investigate whether aftercare treatment consisting of CET combined with acamprosate is equivalent to (A) CET as monotherapy, (B) aftercare as usual (AAU) as monotherapy or (C) AAU combined with acamprosate. METHODS: Patients were randomized to receive either CET with urge-specific coping skills (USCS) as aftercare or AAU. Acamprosate prescription data were extracted from patient case records. Alcohol consumption, cravings, and USCS were assessed at pre-aftercare, post-aftercare, and 6-month follow-up. RESULTS: Overall, patients increased their alcohol consumption during and following aftercare treatment, thereby relapsing despite any treatment. However, CET + acamprosate achieved greater abstinence compared to AAU + acamprosate at follow-up (p=.047). CET + acamprosate also reduced number of drinking days (p=.020) and number of days with excessive drinking (p=.020) at post-aftercare, when compared to AAU monotherapy. CET monotherapy increased sensible drinking at post-aftercare compared to AAU monotherapy (p=.045) and AAU + acamprosate (p=.047). Only CET monotherapy showed improvement in cravings, when compared to AAU at follow-up (mean urge level: p=.032; peak urge level: p=.014). CONCLUSION: The study showed that CET both as monotherapy and combined with acamprosate was superior to AAU monotherapy and AAU + acamprosate in reducing alcohol consumption. Only CET + acamprosate was capable of reducing alcohol consumption in the longer term, indicating that anti-craving medication may not impede CET from exerting an effect on alcohol consumption. Trial registration: ClinicalTrials.gov ID: NCT02298751 (24/11-2014).

Pharmacological enhancing agents targeting cognition in patients with alcohol-induced neurocognitive disorders: A systematic review.

Debilitating neurocognitive deficits are seen in alcohol use disorders (AUD) and Wernicke-Korsakoff's syndrome (WKS). These shared characteristics suggest a spectrum of alcohol-induced neurocognitive disorders (AIND). Cognitive pharmacological enhancing agents (CPEA) have been examined in the treatment of other psychiatric disorders, but little is known about the effects of these agents on AINDs. Our aim was to synthesize the evidence for the effectiveness of CPEAs on AINDs. Databases were searched for controlled trials examining CPEAs on AUD, WKS, and alcohol-related dementia (ARD). Eligible studies were included in a qualitative synthesis and a quality assessment was conducted. The search identified 23 studies (4 ≤ ns ≤ 98). Evidence suggests that modafinil may improve executive functions in AUD and ARD, but this effect may only be present in patients with severe deficits. The studies were rated as having a moderate risk of bias. Despite the promising effects of modafinil, small samples and inconsistent evidence deem the results preliminary. More research is warranted examining the effects of transdiagnostic CPEAs on deficits across AINDs.

A Mobile Phone App Featuring Cue Exposure Therapy As Aftercare for Alcohol Use Disorders: An Investigator-Blinded Randomized Controlled Trial.

BACKGROUND: Cue exposure therapy (CET) is a psychological approach developed to prepare individuals with alcohol use disorder (AUD) for confronting alcohol and associated stimuli in real life. CET has shown promise when treating AUD in group sessions, but it is unknown whether progressing from group sessions to using a mobile phone app is an effective delivery pathway. OBJECTIVE: The objectives of this study were to investigate (1) whether CET as aftercare would increase the effectiveness of primary treatment with cognitive behavior therapy, and (2) whether CET delivered through a mobile phone app would be similarly effective to CET via group sessions. METHODS: A total of 164 individuals with AUD were randomized to one of three groups: CET as group aftercare (CET group), CET as fully automated mobile phone app aftercare (CET app), or aftercare as usual. Study outcomes were assessed face-to-face at preaftercare, postaftercare, and again at 6 months after aftercare treatment. Generalized mixed models were used to compare the trajectories of the groups over time on drinking, cravings, and use of urge-specific coping skills (USCS). RESULTS: In all, 153 of 164 individuals (93%) completed assessments both at posttreatment and 6-month follow-up assessments. No differences in the trajectories of predicted means were found between the experimental groups (CET group and app) compared with aftercare as usual on drinking and craving outcomes over time. Both CET group (predicted mean difference 5.99, SE 2.59, z=2.31, P=.02) and the CET app (predicted mean difference 4.90, SE 2.26, z=2.31, P=.02) showed increased use of USCS compared to aftercare as usual at posttreatment, but this effect was reduced at the 6-month follow-up. No differences were detected between the two experimental CET groups on any outcomes. CONCLUSIONS: CET with USCS delivered as aftercare either via group sessions or a mobile phone app did not increase the effectiveness of primary treatment. This suggests that CET with USCS may not be an effective psychological approach for the aftercare of individuals treated for AUD. TRIAL REGISTRATION: ClinicalTrials.gov NCT02298751; https://clinicaltrials.gov/ct2/show/NCT02298751.