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Non-fatal opioid overdoses are associated with significant morbidity. Hypoxic brain injury caused by opioid-induced respiratory depression is a key mechanism of such morbidity. For example, reports describe an amnestic syndrome in opioid users associated with acute injury to the hippocampus, a brain region that is highly susceptible to hypoxic injury. In our recent study we investigated the effects of non-fatal opioid overdose on the hippocampal volume in a well-characterized sample of opioid use disorder (OUD) patients with a history of overdose (OD) compared to those with no prior overdose (NOD). Using structural magnetic resonance imaging (MRI) and voxel-based morphometry, we observed lower hippocampal volume in patients with a history OD than in the NOD group. These findings support an association between non-fatal opioid overdose and hippocampal injury, which we hypothesize contributes to recently reported cases of OUD related amnestic syndrome. Here we review our study findings and the potential pathophysiological mechanisms underlying the acute and delayed hippocampal injury in nonfatal opioid overdose. We also discuss the implications for the risk of overdose and brain injury with the increased prevalence of fentanyl and xylazine contamination of the illicit opioid supply. Lastly, we highlight considerations for clinical management of the underappreciated neurological injury and cognitive dysfunction in OUD patients. [ABSTRACT FROM AUTHOR]

Incidence of opioid‐related overdoses in the United States has increased dramatically over the past two decades. Despite public emphasis on overdose fatalities, most overdose cases are not fatal. Although there are case reports of amnestic syndromes and acute injury to the hippocampus following non‐fatal opioid overdose, the effects of such overdoses on brain structure are poorly understood. Here, we investigated the neuroanatomical correlates of non‐fatal opioid overdoses by comparing hippocampal volume in opioid use disorder (OUD) patients who had experienced an opioid overdose (OD; N = 17) with those who had not (NOD; N = 32). Voxel‐based morphometry showed lower hippocampal volume in the OD group than in the NOD group, which on post hoc analysis was evident in the left but not the right hippocampus. These findings strengthen the evidence that hippocampal injury is associated with non‐fatal opioid overdose, which is hypothesized to underlie overdose‐related amnestic syndrome. [ABSTRACT FROM AUTHOR]

Background: Excessive consumption of opioids is associated with impaired metabolic function including increased body mass index (BMI). Opioid antagonist naltrexone (NTX) is an effective treatment for opioid use disorder (OUD) that has the potential to mitigate such metabolic disturbances. Understanding the relationship between treatment adherence and BMI in NTX-treated OUD patients may provide valuable insights into optimizing clinical outcomes. Methods: Patients with opioid dependence were offered up to three monthly injections of extended-release (XR) NTX. Treatment completers (n = 41) were defined as those who had received all three XR-NTX injections, and noncompleters (n = 20) as those missing at least one injection. Logistic regression was performed to examine the association between pre-treatment BMI and treatment completion. Results: BMI was positively associated with treatment completion. This association remained significant after adjusting for potentially confounding variables. Conclusion: Our findings suggest that baseline BMI may serve as a potential predictor of XR-NTX treatment adherence in patients with OUD and could help healthcare providers and policy makers alike in developing strategies to improve retention and tailor interventions for specific patient subgroups. [ABSTRACT FROM AUTHOR]

The translocator protein (TSPO) transports cholesterol into mitochondria and is involved in steroidogenesis. The TSPO polymorphism rs6971 influences binding of cholesterol and other TSPO ligands including positron-emission tomography (PET) imaging radiotracers. Although it is recognized that alcohol increases plasma high-density lipoproteins (HDLs), its effects on total cholesterol and triglycerides along with its relationship to TSPO genotype have not been assessed. Here, we evaluated whether plasma cholesterol and triglycerides are disrupted in alcohol use disorder (AUD) and their association with rs6971 in 932 AUD participants (DSM IV or 5) and 546 controls. AUD participants compared with controls had significantly higher plasma levels of total cholesterol, HDL, and triglycerides, but not of low-density lipoprotein (LDL). In the AUD group only, TSPO rs6971 had a significant effect on plasma levels of cholesterol, LDL, and triglycerides (AA (n = 62) > AG (n = 319) > GG (n = 551)), but not on HDL levels. Additionally, we showed a significant effect of TSPO rs6971 on withdrawal scores (Clinical Institute Withdrawal Assessment for Alcohol [CIWA]), with higher scores in AA (n = 50) compared with AG (n = 238) and GG (n = 428). CIWA scores in AUD participants correlated negatively with LDL and positively with HDL, but not with total cholesterol or triglycerides. These findings corroborate elevated plasma cholesterol and HDL levels in AUD and document significant increases in triglycerides. We also reveal for the first time an association in AUD participants between TSPO rs6971 genotype and plasma cholesterol, LDL, and triglyceride levels (not for HDL) and with withdrawal severity. Mediation analyses revealed that LDL (but not HDL) influenced the association between TSPO and alcohol withdrawal severity. [ABSTRACT FROM AUTHOR]

Background and Aims: Although personality traits are implicated in substance use disorders (SUDs) and obesity, differences and similarities between them have not been assessed. Our main aim was to compare personality traits between people with different SUDs, obese people and healthy controls. Design This was a secondary analysis of personality scores obtained from participants in neuroimaging studies from Brookhaven National Laboratory and the Laboratory of Neuroimaging, National Institutes of Health. Setting: United States. Participants/Cases: Individuals with obesity (OB) n = 41, alcohol use disorder (AUD) n = 39, marijuana use disorder (MUD) n = 24, cocaine use disorder (CUD) n = 100, and healthy controls (HC) n = 117 (237 males and 84 females). Measurements The Multidimensional Personality Questionnaire, which characterizes positive emotionality (PEM), negative emotionality (NEM) and constraint (CON) traits. Adjusted covariates included cigarette smoking status, age, gender and body mass index (BMI). Findings Multivariate analysis of covariance showed a main group effect (i.e. OB, AUD, MUD, CUD and HC) only on NEM (P < 0.0001, η2 = 0.17) and CON (P = 0.005, η2 = 0.12). Specifically, NEM was higher in AUD (P < 0.0001, d = 10.4), CUD (P < 0.0001, d = 8.2) and MUD (P = 0.001, d = 9.2), but not in OB (P > 0.05, d = 2.8) relative to HC. CUD showed lower CON (P = 0.015, d = 5.4) and PEM (P = 0.018, d = 4.8) than HC; however, these differences were not significant in the other groups. NEM and CON were negatively correlated for groups combined (r = −0.26, P < 0.0001), and separately for OB (r = −0.49, P = 0.001) and CUD (r = −0.22, P = 0.03). Cigarette smoking status did not influence group differences in NEM, PEM or CON. Conclusions: Compared with healthy controls, people with substance use disorders appear to show higher negative emotionality, and people with cocaine use disorders appear to show lower positive emotionality and constraint traits. Similar findings were not found among people with obesity. [ABSTRACT FROM AUTHOR]

Cognitive bias modification (CBM) was first developed as an experimental tool to examine the causal role of cognitive biases, and later developed into complementary interventions in experimental psychopathology research. CBM involves the “re-training” of implicit biases by means of multiple trials of computerized tasks, and has been demonstrated to change anxious, depressive and drug-seeking behavior, including clinically relevant effects. Recently, the field has progressed by combining CBM with neuroimaging techniques, which provides insight into neural mechanisms underlying how CBM affects implicit biases in anxiety, depression, and addiction, and potentially other pathologies. This narrative literature review summarizes the state of the art of studies on the neural effects of CBM and provides directions for future research in the field. A total of 13 published studies were found and discussed: n = 9 in anxiety, n = 2 in depressive behavior, and n = 2 in addiction. [ABSTRACT FROM AUTHOR]

Alcohol-dependent patients have been shown to faster approach than avoid alcohol stimuli on the Approach Avoidance Task ( AAT). This so-called alcohol approach bias has been associated with increased brain activation in the medial prefrontal cortex and nucleus accumbens. Cognitive bias modification ( CBM) has been used to retrain the approach bias with the clinically relevant effect of decreasing relapse rates one year later. The effects of CBM on neural signatures of approach/avoidance tendencies remain hitherto unknown. In a double-blind placebo-controlled design, 26 alcohol-dependent in-patients were assigned to a CBM or a placebo training group. Both groups performed the AAT for three weeks: in CBM training, patients pushed away 90 percent of alcohol cues; this rate was 50 percent in placebo training. Before and after training, patients performed the AAT offline, and in a 3 T magnetic resonance imaging scanner. The relevant neuroimaging contrast for the alcohol approach bias was the difference between approaching versus avoiding alcohol cues relative to soft drink cues: [(alcohol pull > alcohol push) > (soft drink pull > soft drink push)]. Before training, both groups showed significant alcohol approach bias-related activation in the medial prefrontal cortex. After training, patients in the CBM group showed stronger reductions in medial prefrontal cortex activation compared with the placebo group. Moreover, these reductions correlated with reductions in approach bias scores in the CBM group only. This suggests that CBM affects neural mechanisms involved in the automatic alcohol approach bias, which may be important for the clinical effectiveness of CBM. [ABSTRACT FROM AUTHOR]

Impairment in inhibitory control has been proposed to contribute to habitual alcohol use, abuse and eventually dependence. Moreover, alcohol-dependent (AD) patients have shown a loss of gray matter volume (GMV) in the brain, specifically in prefrontal regions associated with executive functions, including response inhibition. To date, no study has evaluated whether this prefrontal GMV reduction is related to response inhibition in alcohol dependence. To address this issue, we acquired high-resolution T1-weighted magnetic resonance mages from recently detoxified AD patients ( n =22) and healthy controls (HC; n =21). Differences in local GMV between groups were assessed by means of voxel-based morphometry (VBM). Moreover, within the AD group, mean local GMV reductions were extracted and correlated with behavioral performance on the stop-signal task. We found a significantly decrease in GMV in the left inferior frontal gyrus (IFG) in AD patients compared with HC subjects. Further, mean local GMV in this area correlated positively with reaction times on go trials during the stop-signal task in AD patients. Our findings suggest that GMV losses in the IFG in AD patients are related to faster go responses on the stop-signal task. [ABSTRACT FROM AUTHOR]