Acute anxiety states in emergency neuropsychiatry: diagnostic boundaries, time-sensitive mechanisms, and rapid-acting therapeutic strategies

INTRODUCTION: Acute anxiety states (AAS) impose a disproportionate burden on emergency neuropsychiatry. Nevertheless, they remain under-standardized in triage and rapid-phase management and are often misclassified among high-risk medical mimics. AREAS COVERED: This narrative review is based on literature retrieved from PubMed, Embase, ClinicalTrials.gov, and the Cochrane Library (January 2000-September 2026), and addresses diagnostic boundaries, acute versus chronic neurobiological mechanisms, current pharmacotherapy limitations, and emerging rapid-acting agents. This article reconceptualizes AAS as a transdiagnostic, time-sensitive phenotype rather than a discrete nosological entity. It critically appraises DSM-5-TR/ICD-11 diagnostic boundaries, GRACE-1-aligned triage for non-cardiac chest pain, and age-specific screening including 4AT and GAI-SF. The authors review the acute neurobiology distinguishing AAS from trait anxiety - transient glutamatergic-GABAergic remodeling, neurosteroid depletion, non-genomic HPA feedback, and amygdala-PFC-BNST circuit dysregulation - alongside rapid-acting candidates including MM-120 (now redesignated DT120), LYT-300, and subunit-selective GABAkines. EXPERT OPINION: Reflexively discharging AAS after cardiac rule-out perpetuates somatic hypervigilance and forfeits cardiovascular risk mitigation. However, extrapolating provocation-paradigm efficacy of psychoplastogens and pherines to chaotic ED cohorts is premature; regulatory, safety, equity, and false-positive concerns surrounding biomarker-driven closed-loop platforms remain unresolved. Over the next 5-10 years, genuine translational progress will be defined by mechanism-targeted anxiolytics validated in unselected acute-care populations, not by digital phenotyping alone.