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Orbitofrontal sulcogyral morphology in patients with cocaine use disorder.

ABSTRACT: Orbitofrontal cortex (OFC) is thought to be involved in appropriate processing of rewarding stimuli, and abnormal OFC structure and function has been found in patients with substance use disorders. Atypical patterns of the H-sulcus in the OFC have been primarily identified with schizophrenia, but also with bipolar disorder, both of which are associated with comorbid substance use. Given the high rates of substance use within Axis I psychiatric disorders, it is reasonable to consider how frequencies of OFC patterns in populations with only substance use compare to controls. This information is crucial to disentangle whether atypical frequencies of H-sulcus sulcogyral patterns within psychopathology are associated with the psychiatric or substance use phenotype. Here, we present the first analysis of H-sulcus sulcogyral patterns in a population of adult black men with (n = 84) and without (n = 24) cocaine use disorder (CUD). We find that OFC sulcogyral patterns are not significantly different from the control group, indicating that OFC sulcogyral patterns are not disrupted in patients with CUD. As exploratory analyses, we describe OFC sulcogyral pattern subtypes in this cohort as well as an additional control group (n = 52), in order to add to the growing body of literature on OFC sulcogyral pattern characterization.

SUBMITTER: Patti MA

PROVIDER: S-EPMC8126989 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Orbitofrontal sulcogyral morphology is a transdiagnostic indicator of brain dysfunction.

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Project description:Opioid use disorder (OUD) is influenced by genetic and environmental factors. While recent research suggests epigenetic disturbances in OUD, this is mostly limited to DNA methylation (5mC). DNA hydroxymethylation (5hmC) has been widely understudied. We conducted a multi-omics profiling of OUD in a male cohort, integrating neuronal-specific 5mC and 5hmC as well as gene expression profiles from human postmortem orbitofrontal cortex (OUD=12; non-OUD=26). Single locus methylomic analysis and co-methylation analysis showed a higher number of OUD-associated genes and gene networks for 5hmC compared to 5mC; these were enriched for GPCR, Wnt, neurogenesis, and opioid signaling. 5hmC marks also showed a higher correlation with gene expression patterns and enriched for GWAS of psychiatric traits. Drug interaction analysis revealed interactions with opioid-related drugs, some used as OUD treatments. Our multi-omics findings suggest an important role of 5hmC and reveal loci epigenetically dysregulated in OFC neurons of individuals with OUD.

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Project description:OBJECTIVES:This study sought to assess the safety of carvedilol therapy among heart failure (HF) patients with a cocaine-use disorder (CUD). BACKGROUND:Although carvedilol therapy is recommended among certain patients with HF, the safety and efficacy of carvedilol among HF patients with a CUD is unknown. METHODS:This was a single-center study of hospitalized patients with HF. Cocaine use was self-reported or defined as having a positive urine toxicology. Patients were divided by carvedilol prescription. Subgroup analyses were performed by strata of ejection fraction (EF) ?40%, 41% to 49%, or ?50%. Major adverse cardiovascular events (MACE) were defined as cardiovascular mortality and 30-day HF readmission. RESULTS:From a cohort of 2,578 patients hospitalized with HF in 2011, 503 patients with a CUD were identified, among whom 404 (80%) were prescribed carvedilol, and 99 (20%) were not. Both groups had similar characteristics; however, those prescribed carvedilol had a lower LVEF, heart rate, and N-terminal pro-B-type natriuretic peptide concentrations at admission and on discharge, and more coronary artery disease. Over a median follow-up of 19 months, there were 169 MACEs. The MACE rates were similar between the carvedilol and the non-carvedilol groups (32% vs. 38%, respectively; p = 0.16) and between those with a preserved EF (30% vs. 33%, respectively; p = 0.48) and were lower in patients with a reduced EF taking carvedilol (34% vs. 58%, respectively; p = 0.02). In a multivariate model, carvedilol therapy was associated with lower MACE among patients with HF with a CUD (hazard ratio: 0.67; 95% confidence interval; 0.481 to 0.863). CONCLUSIONS:Our findings suggest that carvedilol therapy is safe for patients with HF with a CUD and may be effective among those with a reduced EF.

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Project description:Objective. To systematically assess previous findings on the orbitofrontal sulcogyral pattern in psychiatric disorders and to address the utility of this pattern as a transdiagnostic trait marker of early neurodevelopment in the social brain. Methods. An online literature search was conducted using the PubMed database from inception to August 2019. Studies included in this review were based on the Chiavaras's original classification method of this H-shaped sulcus (type I, II, and III), intermediate orbital sulcus (IOS), and posterior orbital sulcus (POS). Results. Twenty-six studies were included in the review. Sixteen studies (62%) focused on schizophrenia spectrum (Sz) disorders, and the remaining studies focused on autism spectrum disorder (ASD), attention-deficit/hyperactivity disorder (ADHD), history of extremely preterm and extremely low birth weight, bipolar disorder (BD), panic disorder, obsessive-compulsive disorder, cannabis users, and pathological gambling. In Sz, compared with healthy controls, the orbitofrontal sulcogyral pattern was decreased in type I, increased in type II and III, and there were fewer numbers of IOS and POS reported, although specificity in sex and hemispheric dominance was not consistent. BD and neurodevelopmental disorders in ASD and ADHD showed a similar pattern of alteration to that observed in the Sz. Conclusions. The present review of the orbitofrontal sulcogyral pattern indicated that type I expression might reflect a neurodevelopmental protective marker, and type II and III expressions, as well as fewer numbers of IOS and POS, might reflect neurodevelopmental risk markers. These trait markers may be transdiagnostic among socially disabling diseases.

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