BackgroundIn Residential Aged Care Homes (RACHs), medication administration is typically carried out by aged care workers, rather than being under the control of older adults. Very little empirical qualitative evidence exists around situations where medication is refused by older adults.Research aimTo explore aged care workers', older adults', and family members' perspectives and experiences of medication refusal in RACHs.Research designA qualitative exploratory study design. Participants and research contextBetween November 2024 and May 2025, participants were purposively recruited from two RACHs, and through a peak consumer group for people living with dementia and their families. Semi-structured interviews were conducted with aged care workers (n = 10), older adults living in aged care (n = 9), and family members of older adults (n = 7). Data were analysed using Braun and Clarke's reflexive thematic analysis.Ethical considerationsInterview participation was voluntary, with either written or verbal consent obtained, depending on participants' preferences. Identities were replaced with participant type and a numerical code. This study was approved by the Monash University Human Research Ethics Committee (MUHREC) (ID 41475). FindingsThree themes and four subthemes were developed regarding medication refusal in RACHs. These themes encompassed: (1) 'Voices from different corners: medication refusals as more than just saying "no"'; (2) 'the tightrope of role obligations - doing good, respecting choice, and avoiding harm'; and (3) 'Competent to say yes, but not to say no: the erosion of the right to refuse'.ConclusionsMedication refusals in RACHs are clinically and ethically challenging for aged care workers, who use a variety of well-intentioned strategies to respond to these events. Given the complex nature of medication refusals, it is important that aged care workers take older adults' decisional competence into consideration, balancing respect for autonomy with beneficence and best interests decision-making.

Neurogenic pulmonary edema (NPE) is a life-threatening complication of severe central nervous system (CNS) injury. Carbon monoxide (CO) poisoning causes significant CNS insults, including direct neurotoxicity and autonomic dysfunction, creating a high-risk neurological state. Electroconvulsive therapy (ECT), while an effective treatment for severe depression, induces profound physiological stress that can exacerbate underlying neuropathology, thereby increasing the risk of NPE. We present the case of a 62-year-old male with severe depression who was hospitalized after a suicide attempt through CO poisoning, who developed NPE after undergoing his first ECT session. Shortly after the first ECT treatment, the patient became hypertensive, agitated and developed respiratory distress. NPE was diagnosed based on clinical findings and radiographic evidence of prominent pulmonary vasculature. Despite medical management, the patient required emergent intubation and intensive care unit (ICU) management. The patient's condition improved with supportive care, and he was successfully extubated the following day. ECT was discontinued. This case highlights a rare but severe complication of ECT in a patient with pre-existing CNS vulnerability from CO poisoning. The physiological stress from ECT likely precipitated the sympathetic surge leading to NPE. This report underscores the potential dangers of performing ECT after recent CO poisoning and, when considered with the related research discussed herein, suggests that recent CO poisoning should be considered a relative contraindication for ECT. Clinicians must be vigilant about this complication and be prepared for its management.

Serotonergic psychedelics are increasingly investigated as treatments for affective disorders. Concerns persist regarding their potential to induce hypomania or mania, particularly in individuals with bipolar spectrum vulnerability. Whether these substances precipitate transient mood switches or contribute to persistent bipolar illness or diagnostic transition remains unclear. We conducted a systematic review of human studies examining manic or hypomanic symptoms following exposure to serotonergic psychedelics (psilocybin, LSD, mescaline, DMT/ayahuasca) or MDMA (CRD420251160656). Databases and trial registries were searched through January 26, 2026. Eligible designs included randomized and non-randomized clinical studies, registry-based cohorts, cross-sectional surveys, and longitudinal observational studies. Outcomes included dysphoria/euphoria, manic or hypomanic symptoms and transition to bipolar disorder. Risk of bias was assessed using ROBINS-I, ROB2 or NIH tools. Twenty-three studies met inclusion criteria, four contributing to meta-analysis. Rates of psychedelic-associated dysphoria/euphoria, hypomania or mania ranged from 5.8% in controlled trials of psilocybin-assisted psychotherapy for major depressive disorders to 30% in naturalistic studies of individuals with bipolar disorder. When present, manic symptoms were typically acute and self-limited. Observational studies identified higher risks among individuals with bipolar I disorder, familial vulnerability, polysubstance use, and unsupervised or illegal use. Registry-based cohorts examining diagnostic transitions showed a prevalence of subsequent transition to bipolar disorder of 4% (95% CI 2-8%; N = 7478; I[2] = 32.1%), with little evidence for a hallucinogen-specific signal. Overall, serotonergic psychedelics appear to pose a low but clinically meaningful relative risk of transient mood-related symptoms in susceptible individuals while remaining relatively safe in controlled clinical settings. Long-term outcomes and repeated exposure remain insufficiently studied, underscoring the need for rigorous longitudinal research.

Traditional monoaminergic medications often offer limited relief for the physical and cognitive symptoms of post-traumatic stress disorder (PTSD) and complex PTSD. Growing data now point to fast-acting, glutamate-based treatments that boost synaptic plasticity and interrupt fear-conditioned neural circuits. We report four sequential cases of hard-to-treat trauma-spectrum disorders-somatic PTSD, acute bereavement-related PTSD, trauma-linked adolescent depression, and complex PTSD complicated by bipolar II disorder, ADHD, and borderline features-that showed clinically meaningful symptom improvement, typically within days to weeks, with an inexpensive, fully oral protocol centred on dextromethorphan (DXM) potentiated by fluoxetine, with optional add-on piracetam and/or bupropion. All four patients showed notable reductions in intrusive memories, rumination, somatic pain, and functional disability; no episodes of dissociation, hypertension, or mania were clinically documented during follow-up, although structured screening for hypomania/mania and serotonergic toxicity was not performed. These findings are strictly hypothesis-generating and broaden the ketamine/Auvelity framework to trauma-spectrum presentations. They suggest that further controlled investigation into oral NMDA-AMPA modulators may be warranted for trauma-related conditions.

This network meta-analysis evaluates the efficacy and safety of pharmacological and physical treatments for depressive episodes in adolescents with bipolar disorder (BD), incorporating evidence from six randomized controlled trials (RCTs), total N = 879. Due to the absence of shared comparators, pharmacological treatments and non-invasive brain stimulation (NIBS) were analyzed in separate evidence networks rather than being directly compared.Pharmacological treatments included lurasidone, olanzapine-fluoxetine combination (OFC), and quetiapine, while NIBS consisted of transcranial direct current stimulation (tDCS) and intermittent theta-burst stimulation (iTBS). P-scores probabilities showed lurasidone as the most effective for reducing depressive symptoms (CDRS-R SMD: -0.41, 95% CI: -0.62 to -0.19) and improving response rates (RR: 1.64, 95% CI: 1.30-2.04). OFC had the highest remission rates (RR: 1.39, 95% CI: 1.03-1.89). Quetiapine demonstrated limited antidepressant efficacy (CDRS-R SMD: -0.12, 95% CI: -0.38-0.15) but significantly reduced treatment-emergent mania risk (RR: 0.22, 95% CI: 0.05-0.97). In NIBS, tDCS outperformed both iTBS and placebo for reducing depressive (HAMD SMD: -2.56, 95% CI: -3.40 to -1.73) and anxiety symptoms (HAMA SMD: -3.21, 95% CI: -4.15 to -2.28). These results suggest that lurasidone and tDCS may be promising options for symptom management in adolescents with BD, while quetiapine may be considered for preventing manic switching. Further studies, including head-to-head trials, are needed to better understand the long-term effects and address gaps in suicide risk management and multimodal treatment strategies.