buprenorphine and Cognitive-Dysfunction

The number of children with prenatal opioid exposure to medication for addiction treatment (MAT) with methadone and buprenorphine for maternal opioid use disorder is increasing, but the associations of this exposure with cognitive outcomes are not well understood.. To examine the strength and consistency of findings in the medical literature regarding the association of prenatal exposure to MAT with early childhood cognitive development, particularly when accounting for variables outside MAT exposure.. A search strategy obtained publications from PubMed, CINAHL, PsycINFO, Web of Science, and Embase from January 1972 to June 2019. Reference lists from identified articles were searched.. Inclusion criteria were cohort studies, studies including children aged 1 to 60 months with at least 2 months of prenatal MAT exposure, studies using standardized direct-observation testing scales, and studies reporting means and SDs. Case reports, case series, historical controls, and reviews were excluded.. Two authors independently selected studies for inclusion, extracted data, and assessed study quality. Data extracted included demographic characteristics, covariates, sources of bias, and effect estimates. Meta-analysis was performed using random-effects models. This study was conducted according to the Meta-analysis of Observational Studies in Epidemiology (MOOSE) guidelines and the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) statement. Data extraction and synthesis were conducted between January 2018 and August 2019.. Cognitive test scores and demographic variability between exposed and unexposed groups.. A total of 16 unique cohorts, described in 27 articles and including 1086 children (485 [44.7%] with MAT exposure), were included in a quantitative synthesis. On meta-analysis, MAT exposure was associated with lower cognitive development scores (pooled standardized mean difference, -0.57; 95% CI, -0.93 to -0.21; I2 = 81%). Multiple subanalyses on demographic characteristics (ie, maternal education, race/ethnicity, socioeconomic status, prenatal tobacco exposure, infant sex) were conducted. In the subanalysis of studies with comparable prenatal exposure to tobacco smoke, the association of MAT exposure with cognitive scores was no longer statistically significant and became homogeneous (standardized mean difference, -0.11; 95% CI, -0.42 to 0.20; I2 = 0%).. In this study, predefined subanalyses demonstrated how poor recruitment, particularly imbalances in maternal tobacco use, could contribute to a negative overall association of cognitive development test scores with prenatal MAT exposure. Promoting tobacco cessation for pregnant women with opioid use disorder should be prioritized in this high-risk population.

Topics: Analgesics, Opioid; Buprenorphine; Child Development; Child, Preschool; Cognition; Cognitive Dysfunction; Female; Humans; Infant; Infant, Newborn; Male; Maternal Exposure; Methadone; Opiate Substitution Treatment; Opioid-Related Disorders; Pregnancy; Pregnancy Complications; Prenatal Exposure Delayed Effects; Risk Factors

Cognitive dysfunction is disproportionately prevalent among persons with opioid use disorder (OUD). Specific domains of cognitive dysfunction (attention, executive functioning, memory, and information processing) may significantly impede treatment outcomes among patients on medication for OUD (MOUD). This limits patient's ability to learn, retain, and apply information conveyed in behavioral intervention sessions. Evidence-based accommodation strategies have been integrated into behavioral interventions for other patient populations with similar cognitive profiles as persons with OUD; however, the feasibility and efficacy of these strategies have not yet been tested among patients on MOUD in a drug treatment setting.. We conducted a series of focus groups with 25 key informants (10 drug treatment providers and 15 patients on MOUD) in a drug treatment program in New Haven, CT. Using an inductive approach, we examined how cognitive dysfunction impedes participant's ability to retain, recall, and utilize HIV prevention information in the context of drug treatment.. Two main themes capture the overall responses of the key informants: (1) cognitive dysfunction issues and (2) accommodation strategy suggestions. Subthemes of accommodation strategies involved suggestions about particular evidence-based strategies that should be integrated into behavioral interventions for persons on MOUD. Specific accommodation strategies included: use of a written agenda, mindfulness meditation, multi-modal presentation of information, hands-on demonstrations, and a formal closure/summary of sessions.. Accommodation strategies to compensate for cognitive dysfunction were endorsed by both treatment providers and patients on MOUD. These accommodation strategies have the potential to enhance the efficacy of behavioral interventions to reduce HIV transmission among persons on MOUD as well as addiction severity, and overdose.

Topics: Buprenorphine; Cognition; Cognitive Dysfunction; HIV Infections; Humans; Opioid-Related Disorders

Approximately 15-40% of people living with HIV develop HIV-associated neurocognitive disorders, HAND, despite successful antiretroviral therapy. There are no therapies to treat these disorders. HIV enters the CNS early after infection, in part by transmigration of infected monocytes. Currently, there is a major opioid epidemic in the United States. Opioid use disorder in the context of HIV infection is important because studies show that opioids exacerbate HIV-mediated neuroinflammation that may contribute to more severe cognitive deficits. Buprenorphine is an opioid derivate commonly prescribed for opiate agonist treatment. We used the EcoHIV mouse model to study the effects of buprenorphine on cognitive impairment and to correlate these with monocyte migration into the CNS. We show that buprenorphine treatment prior to mouse EcoHIV infection prevents the development of cognitive impairment, in part, by decreased accumulation of monocytes in the brain. We propose that buprenorphine has a novel therapeutic benefit of limiting the development of neurocognitive impairment in HIV-infected opioid abusers as well as in nonabusers, in addition to decreasing the use of harmful opioids. Buprenorphine may also be used in combination with HIV prevention strategies such as pre-exposure prophylaxis because of its safety profile.

Topics: AIDS Dementia Complex; Animals; Antigens, Ly; Brain; Buprenorphine; Chronic Disease; Cognitive Dysfunction; Disease Models, Animal; HIV Infections; Inflammation; Male; Mice, Inbred C57BL; Monocytes; Phenotype; Viral Load