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1.
Psychiatry Res ; 326: 115340, 2023 Aug.
Article in English | MEDLINE | ID: mdl-37454610

ABSTRACT

Tobacco smoking is a significant determinant of preventable morbidity and mortality worldwide. It is now possible to modulate the activity of the neurocircuitry associated with nicotine dependence using repetitive Transcranial Magnetic Stimulation (rTMS), a non-invasive neurostimulation approach, which has recently demonstrated efficacy in clinical trials and received regulatory approval in the US and Canada. However there remains a paucity of replication studies and real-world patient effectiveness data as access to this intervention is extremely limited. There are a number of unique challenges related to the delivery of rTMS that need to be addressed prior to widespread adoption and implementation of this treatment modality for smoking cessation. In this paper, we review the accessibility, scientific, technological, economical, and social challenges that remain before this treatment can be translated into clinical practice. By addressing these remaining barriers and scientific challenges with rTMS for smoking cessation and delineating implementation strategies, we can greatly reduce the burden of tobacco-related disease worldwide.

2.
J Dual Diagn ; 19(2-3): 71-96, 2023.
Article in English | MEDLINE | ID: mdl-37450645

ABSTRACT

Objective: Cannabis use is increasingly normalized; psychosis is a major adverse health outcome. We reviewed evidence on cannabis use-related risk factors for psychosis outcomes at different stages toward recommendations for risk reduction by individuals involved in cannabis use. Methods: We searched primary databases for pertinent literature/data 2016 onward, principally relying on reviews and high-quality studies which were narratively summarized and quality-graded; recommendations were developed by international expert consensus. Results: Genetic risks, and mental health/substance use problem histories elevate the risks for cannabis-related psychosis. Early age-of-use-onset, frequency-of-use, product composition (i.e., THC potency), use mode and other substance co-use all influence psychosis risks; the protective effects of CBD are uncertain. Continuous cannabis use may adversely affect psychosis-related treatment and medication effects. Risk factor combinations further amplify the odds of adverse psychosis outcomes. Conclusions: Reductions in the identified cannabis-related risks factors-short of abstinence-may decrease risks of related adverse psychosis outcomes, and thereby protect cannabis users' health.


Subject(s)
Cannabis , Psychotic Disorders , Substance-Related Disorders , Humans , Cannabis/adverse effects , Mental Health , Psychotic Disorders/therapy , Risk Factors
3.
Drug Alcohol Depend ; 239: 109604, 2022 10 01.
Article in English | MEDLINE | ID: mdl-36037586

ABSTRACT

BACKGROUND: Craving reduction is an important target in the treatment of prescription-type opioid use disorder (POUD). In this exploratory analysis, we compared the effectiveness of BUP/NX flexible model of care relative to methadone for craving reduction in individuals with POUD. METHODS: We analyzed data from a multicentric, pragmatic, 24-week open-label randomized controlled trial conducted in participants with POUD (N = 272) who were randomly assigned to BUP/NX model of care with flexible take-home dosing (n = 138) or the standard model of care with closely supervised methadone (n = 134). Treatments were prescribed and administered according to local guidelines, in diverse clinical settings. Craving was measured using the Brief Substance Craving Scale at baseline, week 2, 6, 10, 14, 18 and 22. RESULTS: Cravings decreased in both treatment groups over 22 weeks (BUP/NX adjusted mean difference = -5.52, 95% CI = -6.91 to -4.13; methadone adjusted mean difference = -3.95, 95% CI = -5.28 to -2.63; p < 0.001), and were overall lower in the BUP/NX group (adjusted mean = 4.04, 95% CI = 3.43-4.64) than the methadone group (adjusted mean = 5.13, 95% CI = 4.51-5.74; p < 0.001). The time by treatment group interaction (favoring BUP/NX) was statistically significant at week 2 (adjusted mean difference = -1.58, 95% CI = -3.13 to -0.03; p = 0.041). CONCLUSIONS: Compared to the standard methadone model of care, flexible take-home dosing of BUP/NX was associated with lower craving in individuals with POUD. These findings can contribute to guiding shared decision-making regarding OAT treatment in this population.


Subject(s)
Buprenorphine , Opioid-Related Disorders , Buprenorphine/therapeutic use , Buprenorphine, Naloxone Drug Combination/therapeutic use , Craving , Humans , Methadone/therapeutic use , Naloxone/therapeutic use , Narcotic Antagonists/therapeutic use , Opiate Substitution Treatment/methods , Opioid-Related Disorders/drug therapy , Opioid-Related Disorders/rehabilitation , Prescriptions
4.
Sci Rep ; 7(1): 5276, 2017 07 13.
Article in English | MEDLINE | ID: mdl-28706262

ABSTRACT

Previous studies have demonstrated that alcohol consumption impairs neuroplasticity in the motor cortex. However, it is unknown whether alcohol produces a similar impairment of neuroplasticity in the dorsolateral prefrontal cortex (DLPFC), a brain region that plays an important role in cognitive functioning. The aim of the current study was to evaluate the effect of alcohol intoxication on neuroplasticity in the DLPFC. Paired associative stimulation (PAS) combined with electroencephalography (EEG) was used for the induction and measurement of associative LTP-like neuroplasticity in the DLPFC. Fifteen healthy subjects were administered PAS to the DLPFC following consumption of an alcohol (1.5 g/l of body water) or placebo beverage in a within-subject cross-over design. PAS induced neuroplasticity was indexed up to 60 minutes following PAS. Additionally, the effect of alcohol on PAS-induced potentiation of theta-gamma coupling (an index associated with learning and memory) was examined prior to and following PAS. Alcohol consumption resulted in a significant impairment of mean (t = 2.456, df = 13, p = 0.029) and maximum potentiation (t = -2.945, df = 13, p = 0.011) compared to the placebo beverage in the DLPFC and globally. Alcohol also suppressed the potentiation of theta-gamma coupling by PAS. Findings from the present study provide a potential neurophysiological mechanism for impairment of cognitive functioning by alcohol.


Subject(s)
Alcoholic Intoxication/pathology , Ethanol/adverse effects , Evoked Potentials, Motor/drug effects , Neuronal Plasticity , Prefrontal Cortex/pathology , Adult , Alcoholic Intoxication/etiology , Central Nervous System Depressants/adverse effects , Cross-Over Studies , Female , Humans , Male , Middle Aged , Prefrontal Cortex/drug effects , Transcranial Magnetic Stimulation , Young Adult
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