Substance use disorders (SUDs) are a major global health burden, and psychedelic-assisted therapies are now gaining scientific interest, with ibogaine being considered as a candidate for anti-addictive effects across multiple substance classes. Ibogaine is a multi-target indole alkaloid acting on opioid, glutamatergic, serotonergic, and sigma systems with potential to rapidly reduce withdrawal and cravings after a single administration. Ibogaine is metabolized into noribogaine, which has a longer half-life and contributes to sustained pharmacological effects. These compounds act on multiple neurotransmitter systems including NMDA receptors, serotonin receptors, and opioid receptors, which allow it to have a broad neurobiological effect. It also has anti-addictive properties linked to neuroplasticity, dopamine modulation, and opioid receptor activity. Additionally, iboga has use in African rituals, with modern interest increasing in the twentieth century. Ibogaine now is an unregulated or semi-regulated substance with increased interest in controlled clinical development as well. Clinical evidence for ibogaine comes from observational studies and case reports, e.g., particularly in opioid use disorder. Ibogaine carries significant risks, particularly cardiotoxicity, neurological adverse effects including hallucinations, and reported fatalities. Safer derivates such as noribogaine and tabernanthalog (TBG) are being developed to retain anti-addictive efficacy and reduce toxicity. Ibogaine induces prolonged oneirogenic states involved in autobiographical memory processing, and outcomes are influenced by setting, integration therapy, and psychotherapy. Current research is largely observational, and studies are small, which highlights the need for standardized protocols and clinical trials. Overall, ibogaine represents a therapeutic candidate for SUDs, with broad anti-addictive potential. In this review, we provide an overview of ibogaine’s history and pharmacology, critically examine its therapeutic potential in multiple SUDs, and discuss current limitations, emerging alternatives, and future directions.

Substance use disorders are an increasing concern globally, causing a tremendous uptick in public health burden in recent years. Despite the growing attention these disorders receive, there remain no approved pharmacotherapies for stimulant use disorder, thereby contributing a major portion of this burden. This review examines the potential use of Brixadi, an extended-release injectable formulation of the widely used pharmacotherapy buprenorphine, indicated for opioid use disorder, in the treatment of stimulant use disorder. Psychostimulants, including cocaine, methamphetamine, and designer stimulants, all exert their effects by inhibiting or reversing the directionality of the monoamine transporters in the synaptic cleft. Inhibition or reversal of these transporters in the synaptic cleft allows dopamine, serotonin, and norepinephrine to remain in the synapse, which ultimately enhances their activity and contributes to the reinforcement of substance use. The reinforcement loop driven by excess neurotransmitters, particularly dopamine, provides a pharmacotherapeutic target via receptor interactions. Brixadi is an injectable extended-release buprenorphine primarily used to treat opioid use disorder. The extended-release mechanism enables sustained drug-receptor interaction, resulting in stable plasma drug concentrations. Buprenorphine is as a dual-acting agent, a partial μ-opioid receptor (MOR) agonist and a κ-opioid receptor (KOR) antagonist. KOR antagonism modulates symptoms of withdrawal in OUD, including dysphoria, stress, and drug cravings. Therefore, Brixadi’s KOR antagonism may offer a promising pharmacologic target for stimulant use disorder recovery by mitigating these negative affective states. Additionally, the bimodal mechanism suggests that Brixadi may be a beneficial pharmacologic candidate for people who suffer from polysubstance use involving opioids and psychostimulants. While there is promise behind these developments, current studies are limited to preclinical trials and have not yet advanced toward clinical trials. However, Brixadi’s extended-release profile and potential capability to minimize withdrawal-related dysphoria and stress-induced drug seeking present promise for further clinical investigation.

Objectives: This prospective study aimed to assess noise levels in otolaryngology operating rooms (OR), explore noise variation across subspecialties, and examine the correlation between noise, verbal communication, and surgery complexity. Study Design: Prospective trial. Setting: Single academic institution. Methods: Noise levels and surgeon feedback from 60 otolaryngology surgeries at a Tertiary Academic Medical Center were collected between May 2023 and March 2024. Cases were randomly selected based on staff availability, excluding emergency surgeries. The cohort included 13 general ENT, 13 facial plastics, 8 head and neck, 13 laryngology, and 13 rhinology surgeries. Noise data was recorded with a Curconsa Sound Level Meter SL720. Surgeons reported communication ease and case complexity via survey, with communication deemed impaired with the incidence of repeated information in the OR. Case complexity was rated from grade 1 (lowest) to grade 4 (highest). Results: Noise differences between subspecialties’ ORs were statistically significant (p < 0.001), but the Effect size was small (η² ≈ 0.04). The Rhinology OR showed higher average noise levels compared to Facial Plastic (Rhinology louder by ~2.2 dB) and Head-Neck (Rhinology louder by ~2.6 dB). Noise did not significantly impair communication in the OR (p=0.526). Higher noise in the OR did not significantly influence surgical complexity (p=0.547). Conclusion: Noise levels in otolaryngology operating rooms varied modestly across subspecialties. No significant association between noise levels and either communication impairment or surgical complexity was observed.

Background/Objectives: This prospective study aimed to assess noise levels in otolaryngology operating rooms (OR), explore noise variation across subspecialties, and examine the correlation between noise, verbal communication, and surgery complexity. Methods: Prospective observational study. Single academic institution. Noise levels and surgeon feedback from 60 otolaryngology surgeries at a Tertiary Academic Medical Center were collected between May 2023 and March 2024. Cases were prospectively enrolled using a convenience sampling based on research staff availability, excluding emergency surgeries. The cohort included 13 general ENT, 13 facial plastics, 8 head and neck, 13 laryngology, and 13 rhinology surgeries. Noise data was recorded with a Curconsa Sound Level Meter SL720. Surgeons reported communication ease and case complexity via survey, with communication deemed impaired with the incidence of repeated information in the OR. Case complexity was rated from grade 1 (lowest) to grade 4 (highest). Results: Noise differences between subspecialties’ ORs were statistically significant (p < 0.001) but the effect size was small (η² ≈ 0.04). The Rhinology OR showed higher average noise levels compared to Facial Plastic (Rhinology louder by 2.2 dB) and Head–Neck (Rhinology louder by 2.6 dB). Noise did not significantly impair communication in the OR (p = 0.526). Higher noise in the OR did not significantly influence surgical complexity (p = 0.547). Conclusions: Noise levels in otolaryngology operating rooms varied modestly across subspecialties. No significant association between noise levels and either communication impairment or surgical complexity was observed.

Neurodegenerative diseases are targets for pridopidine therapy, which aims to improve quality of life through neuroprotective mechanisms that involve sigma-1 receptor (S1R) activation. Neurodegenerative motor and cognitive diseases are influenced by dopamine imbalance, where disruptions in pathways contribute to states that are hyperkinetic or hypokinetic, while current dopaminergic treatments are symptomatic rather than disease-modifying, especially for Huntington’s disease and Amyotrophic lateral sclerosis. This review summarizes the mechanisms underlying pridopidine-mediated neuroprotection and examines the current evidence supporting its therapeutic potential. The S1R is an endoplasmic reticulum-mitochondria-associated chaperone involved in homeostasis of calcium, stress regulation, and mitochondrial function. Pridopidine is a small lipophilic molecule that crosses the blood–brain barrier and acts as an S1R agonist, with minimal dopamine D2 receptor occupancy. Activation of S1R by pridopidine modulates calcium signaling and enhances anti-apoptotic activity. Collectively, available evidence suggests that pridopidine may improve motor outcomes and slow disease progression in Huntington’s disease and amyotrophic lateral sclerosis, supporting its promise as a disease-modifying therapeutic strategy.