Opioid use disorder (OUD) is highly prevalent in correctional settings, where assessment occurs under conditions of stress, surveillance, and timeconstraint. Under these conditions, fluctuating or inconsistent self-report is common and is frequently interpreted as deception, with consequences for documentation, treatment access, and patient safety. This article develops a conceptual framework for interpreting such response variability without presuming intentional dishonesty, and operationalizes it into a structured interpretive tool for real-time clinical use. The framework draws on three literatures: correctional health and OUD assessment, forensic work on malingering, and quantum cognition research on judgment under uncertainty. Constructs from this synthesis were mapped to recurring patterns observed in correctional OUD assessment. Four quantum cognition constructs (order effects, contextuality, superposition, and interference) account for commonly observed patterns, including environment-dependent disclosure, shifts in withdrawal reporting, and ambivalence toward opioid agonist therapy (OAT). These constructs are translated into a structured interpretive tool that prompts clinicians to consider nondeceptive mechanisms (order, context, motivation, and emotional state) before attributing variability to malingering. Applied at the point of care, the framework supports safer withdrawal management, clearer documentation, and more equitable OAT access in correctional environments.

Objective: Mental and behavioral disorders due to psychoactive substance use, as defined by ICD-10 codes F10-F19, include a spectrum of substance use disorders such as acute intoxication, withdrawal, harmful use, and dependence related to alcohol, opioids, stimulants, cannabis, tobacco, and other substances. These conditions significantly increase the risk of suicide, yet national trends in suicide-related mortality among affected individuals remain underexplored. This study aimed to evaluate national trends in suicide and self-harm mortality among individuals with these disorders from 1999 to 2023. Methods: We conducted a retrospective analysis of U.S. death certificate data from the CDC Wide-ranging Online Data for Epidemiologic Research (WONDER) database (1999-2023). Decedents with mental and behavioral disorders due to psychoactive substance use were identified using ICD-10 codes F10-F19, encompassing acute intoxication, withdrawal, harmful use, and dependence. Suicide and self-harm deaths were defined by ICD-10 codes U03, X60-X84, and Y87. Age-adjusted mortality rates (AAMRs) per million and average annual percentage changes (AAPCs) were estimated using Joinpoint regression. Analyses were stratified by sex, age, race/ethnicity, and metropolitan status. Results: Between 1999 and 2023, 37,473 suicide-related deaths were identified among U.S. individuals with mental and behavioral disorders due to psychoactive substance use. AAMRs increased from 2.2 to 5.7 per million (AAPC: 3.31; p < .01). Males had higher mortality than females (6.6 vs. 2.9), though females had a steeper rate of increase over time. Middle-aged adults had the highest AAMR (8.2), followed by younger (6.9), older adults (3.4) and children and adolescents (1.1). Non-Hispanic (NH) American Indian/Alaska Native individuals (AI/AN) had the highest AAMR (13.5), followed by NH White (6.2), Hispanic/Latino (1.6), NH Black (1.6), and NH Asian/Pacific Islander (API) (1.4). From 1999 to 2000, non-metropolitan areas had higher AAMRs than metropolitan areas (6.5 vs. 4.3), with significant increases in both settings. Conclusions: Suicide-related mortality among individuals with mental and behavioral disorders due to psychoactive substance use has increased significantly increased in the United States from 1999 to 2023, demonstrating substantial disparities by sex, age, race/ethnicity, and geographic region. These findings highlight the critical need for integrated approaches in suicide prevention and substance-related treatment settings.

Dysregulation of the dynorphin (DYN) / kappa-opioid receptor (KOR) system is heavily implicated in symptoms of alcohol use disorder (AUD) including negative affective-like states that can drive maladaptive behavioral regulation. Substantial efforts have been made towards understanding the neurobiology of DYN / KOR dysregulation; however, the role of dynorphinergic islands of Calleja within the ventral striatum remain poorly understood. Presently, adult male Wistar rats were trained to self-administer 10% alcohol, exposed to either air or alcohol vapor for eight weeks, and alcohol self-administration and 22-kHz ultrasonic vocalizations (USVs) assessed during acute withdrawal. Subsequently, brains were extracted during acute withdrawal and DYN A-like immunoreactivity was measured in the ventral striatum. Alcohol vapor-exposed rats demonstrated increased alcohol consumption and 22-kHz USVs compared to air-exposed controls. Vapor-exposed rats additionally demonstrated increased DYN A-like immunoreactivity in the islands of Calleja. Moreover, the average DYN A neuron size positively correlated with the number of 22-kHz USVs in vapor exposed animals, but not in air-exposed controls. The present findings identify the islands of Calleja as a novel DYN-associated region that may be recruited during alcohol dependence with enhanced DYN plasticity in the islands of Calleja contributing to affective dysregulation in AUD and other neuropsychiatric conditions.

Alcohol addiction is a chronically relapsing disorder, characterized by compulsive alcohol seeking and taking, the loss of control in limiting intake, and the emergence of hyperkatifeia (a sensitized negative emotional state) during withdrawal. The hypothesis of this review is that alcohol addiction represents a break with homeostatic brain regulatory mechanisms that regulate the emotional state of the individual via three stages of the addiction cycle and three respective domains of dysfunction. As addiction develops, the withdrawal/negative affect stage, which mediates the development of a panoply of negative emotional symptoms (termed hyperkatifeia), takes on a more prominent role. Hyperkatifeia then drives compulsive-like drug seeking via negative reinforcement and is mediated by a decrease in the function of brain reward systems that involve key neurotransmitter systems, such as dopamine and opioid peptides, and the recruitment/sensitization of brain stress systems, including corticotropin-releasing factor, dynorphin, hypocretin, ghrelin, norepinephrine, and neuroimmune modulation. These changes are hypothesized to be triggered and maintained by neuroadaptations of the hypothalamic-pituitary-adrenal axis and the sensitization of glucocorticoid receptor signaling. Anti-stress systems, such as neuropeptide Y, nociceptin, endocannabinoids, and oxytocin, may be compromised and contribute to the development and maintenance of hyperkatifeia. Neuroanatomical substrates for hyperkatifeia have a focus on the extended amygdala and elements of the basal ganglia. Neurocircuitry analyses are now identifying cellular and molecular targets for genetic and epigenetic vulnerability within an allostasis framework that shows therapeutic promise for this often-neglected domain of the etiology and perpetuation of alcohol addiction.

Hospitalized patients with opioid use disorder present unique clinical challenges, including higher rates of patient-directed discharge (PDD), incomplete treatment courses, and frequent readmissions. To compare outcomes in hospitalized patient encounters involving OUD and bacteremia that were ordered medications for opioid use disorder versus high-dose opioid agonist therapy (HDOAT) alone. This single-center, retrospective study included 268 OUD patients, 383 encounters, and 303 cases of bacteremia admitted to Temple University Hospital from Jan 1, 2020 through Dec 31, 2022. Outcomes of interest included PDD, 7 and 30-day readmission, inpatient mortality, length of stay (LOS), one year mortality and antibiotic completion. Bacteremia is a serious illness and requires long term treatment, thus it is an optimal model for this work. Of 383 encounters, 234 involved MOUD, and 149 involved HDOAT alone. Among the HDOAT group, doses were up to 2,070 MMEs/day. MOUD included buprenorphine and methadone. HDOAT included non-MOUD full agonist such as oxycodone and/or hydromorphone. For case-level outcomes, MOUD was associated with higher antibiotic completion (35.0% vs 23.3%, OR 1.77, p < 0.05). For encounter-level outcomes, MOUD was associated with lower PDD rates (38.5% vs 69.8%, OR 0.27, p < 0.0001) and longer LOS (8d vs 3d), seven-days readmission and inpatient mortality rates were similar between groups. However, 30-day readmission rate was lower in the MOUD group (32.9% vs 43.0%, OR 0.65, p < 0.05). PDD, readmission and mortality were similar regardless of timing of MOUD initiation (<72 h vs > 72h) or severity of opioid dependence. Notably, 23% of HDOAT cases successfully completed antibiotics, often across multiple encounters. MOUD initiation was associated with lower PDD and higher antibiotic completion rates. Timing of MOUD initiation did not affect outcomes. HDOAT may serve as a second-line approach to support continuity of care in patients declining MOUD.

Limited data indicate that hydromorphone is excreted into breastmilk in small amounts, but large maternal dosages have caused neonatal central nervous system depression. In general, maternal use of oral narcotics during breastfeeding can cause infant drowsiness, central nervous system depression and even death. Hydromorphone use should be limited in nursing mothers.[1] Newborn infants seem to be particularly sensitive to the effects of even small dosages of narcotic analgesics. Once the mother's milk comes in, it is best to provide pain control with a nonnarcotic analgesic and limit maternal intake of hydromorphone to a few days at a low dosage with close infant monitoring. If the baby shows signs of increased sleepiness (more than usual), difficulty breastfeeding, breathing difficulties, or limpness, a physician should be contacted immediately.

Maternal use of oral opioids during breastfeeding can cause infant drowsiness, which may progress to rare but severe central nervous system depression.[1,2] Newborn infants seem to be particularly sensitive to the effects of even small dosages of narcotic analgesics. If the mother of a newborn requires codeine, it is not a reason to discontinue breastfeeding; however, once the mother's milk comes in, it is best to provide pain control with a nonnarcotic analgesic and limit maternal intake of oral codeine to 2 to 3 days at a low dosage with close infant monitoring, especially in the outpatient setting.[2-4] If the baby shows signs of increased sleepiness (more than usual), difficulty breastfeeding, breathing difficulties, or limpness, a physician should be contacted immediately.[5] Excessive sedation in the mother often correlates with excess sedation in the breastfed infant. Following these precautions can lower the risk of neonatal sedation.[6] Withdrawal symptoms can occur in breastfed infants when maternal administration of an opioid analgesic is stopped, or when breastfeeding is stopped. Numerous professional organizations and regulatory agencies recommend that other agents are preferred over codeine or to avoid codeine completely during breastfeeding;[7-11] however, a large population study did not find codeine to be more dangerous than other opioids that have been studied less and may not be safer.[12-14]