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

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. 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. 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.