When Do Physical Symptoms After Antidepressant Cessation Reflect Pharmacodynamic versus Non-pharmacodynamic Clinical Phenomena?

Attention has been growing within the scientific literature and lay media about the frequency, extent, severity, and possible long-term ramifications of physical and emotional symptoms¹ associated with stopping serotonergic antidepressants. These phenomena have been construed as antidepressant “discontinuation symptoms” or “withdrawal syndromes.” The term withdrawal, however, can be misleading because it risks conflation with processes associated with addiction. Although both withdrawal and discontinuation effects can cause distressing physical symptoms, monoaminergic antidepressants do not produce reward-related euphoria or craving, lack abuse liability, and do not frequently require escalating doses because of physiological tolerance. Nonetheless, the distinction between withdrawal and discontinuation remains the subject of impassioned debate.² For clarity, the terms discontinuation phenomena or discontinuation symptoms rather than withdrawal are used in the current article. Our intent is to focus on (1) descriptive symptom phenomenology and evaluative/management strategies to minimize potential discomfort during antidepressant treatment cessation and (2) possible explanations for physiologically unusual, delayed, or protracted symptoms in patients for whom non-pharmacodynamic features may be contributory, based on the authors’ collective distillation of pertinent clinical literature.

Discontinuation Symptoms: Phenomenology

Meta-analyses estimate a placebo-subtracted incidence of about 8%³–28%⁴ for physical discontinuation symptoms among individuals with major depressive disorder (MDD) or anxiety disorders who abruptly stop a short half-life selective serotonin reuptake inhibitor (SSRI) or serotonin-norepinephrine reuptake inhibitor (SNRI) after >1 month of treatment. Symptoms usually resolve within 1–2 weeks^4-6 and typically involve dizziness, nausea, vertigo, or nervousness, rather than signs of affective relapse,⁶ encapsulated elsewhere by the mnemonic “FINISH“ (Flu-like symptoms, Insomnia, Nausea, Imbalance, Sensory disturbances [eg, “brain zaps”] and Hyperarousal).⁵ Such putative discontinuation symptoms have been proposed to derive from abrupt changes in serotonin function after SSRI or SNRI discontinuation as well as noradrenergic and cholinergic mechanisms provoked by discontinuation of some SSRIs such as paroxetine.⁷ Risk appears higher in women, younger patients, and those experiencing more adverse effects during treatment and correlates with higher antidepressant doses, short drug half-lives, and longer treatment durations,⁶ although the latter feature has conflicting findings in the literature.^5,8 Eventual recurrences of depression or anxiety may correlate with antidepressant discontinuation phenomena according to some reports, but findings are not definitive.⁸ An important limitation of existing literature is the relatively short duration of follow-up periods (mostly <6 months) for tracking both discontinuation phenomena and relapse of the psychiatric condition for which pharmacotherapy had been initiated.

 Pharmacodynamic, Pharmacokinetic, and Pharmacogenetic Considerations

To minimize physical symptoms after antidepressant cessation, several pharmacologic principles are relevant:

• Half-life duration and other pharmacokinetic factors: Agents with relatively long terminal elimination half-lives (eg, fluoxetine) may auto-taper with lower expectancy of discontinuation phenomena or needing protracted tapers.⁹ Switching from short half-life antidepressants to fluoxetine as a “bridge” transition may help avert discontinuation phenomena.¹⁰ This strategy has not been validated through randomized trials, but remains widely employed in clinical practice based largely on pharmacokinetic rationale and accumulated clinical experience. Paroxetine and venlafaxine are specifically implicated as most likely to provoke discontinuation symptoms due to their short half-lives.⁴ Non-linear pharmacokinetics may also be a factor in high rates of paroxetine discontinuation symptoms; ie, disproportionate drops in blood levels create a “cliff-edge” effect during dose reductions.¹¹
  Product labels for antidepressants generally advise gradual dose reductions rather than abrupt cessations, but without specific timeframes. An exception is vortioxetine, where a 1-step 1-week taper is recommended for doses of 15 or 20 mg/day followed by discontinuation without further tapering.¹²
• Pharmacogenetics: Ultrarapid metabolizers for relevant cytochrome P450 isoenzymes may, theoretically, be at greater risk for more pronounced discontinuation phenomena due to accelerated clearance or inter-dose withdrawal.¹³ Individuals with variants of the 5HT1A receptor gene have also shown greater susceptibility to discontinuation symptoms when stopping paroxetine.¹⁴
• Non-serotonergic antidepressant effects: Antagonism of alpha-1, histamine-1, or anticholinergic receptors could cause rebound effects that further exacerbate discontinuation phenomena. Rebound cholinergic effects are especially a risk when stopping paroxetine.⁷

Proposed Treatment Approaches to Antidepressant Discontinuation

• Slow tapering: In general, slow tapers (defined by some as >4 weeks)¹⁵ may mitigate discontinuation phenomena and relapse risks¹² better than fast tapers (operationalized as <4 weeks), although meta-analyses report no significant differences between “fast” and “slow” tapers in incident rates of discontinuation symptoms.⁴ A 6-month randomized antidepressant discontinuation trial in patients with remitted MDD found no clear relationship between tapering rate and either discontinuation symptoms or eventual relapse rates.⁸ Few if any studies report tapering periods >2 months. Additionally, in the absence of adequate psychological support, relapse rates may be higher despite slow tapers.¹⁵ We could find no systematic studies examining whether slower tapers (with or without psychological support) mitigate discontinuation phenomena more successfully than do faster tapers (with or without psychological support).
• Hyperbolic tapering: This proposed concept hypothesizes that receptor occupancy curves for the serotonin transporter (SERT) are nonlinear and become steeper as antidepressant doses become progressively lower. Consequently, incrementally smaller dosage reductions are theoretically needed at the lower end of a taper to avoid disproportionate decreases in binding consequences.¹⁶ Several limitations bear on linking this theory with pharmacodynamic effects: (1) randomized controlled trials have not yet compared hyperbolic to slow antidepressant tapering (but some are ongoing: eg, https://clinicaltrials.gov/study/NCT07393919); (2) existing neuroimaging studies of SERT receptor binding and SSRI dosing involve small sample sizes; larger samples might reveal greater variability¹⁷; (3) although SSRI doses exhibit a hyperbolic relationship with SERT occupancy, the extent to which this target-occupancy relationship translates into clinical efficacy, adverse effects, or discontinuation symptoms remains incompletely understood; (4) there are no clinical or in vivo human studies demonstrating a contemporaneous association between putative antidepressant discontinuation symptoms and SERT occupancy; and (5) the hypothesis that discontinuation phenomena result from SERT binding fails to consider activity at postsynaptic serotonergic or other interfacing receptors.
• Alternative antidepressant substitution: At least theoretically, transitioning from one agent to another when both inhibit SERT is unlikely to trigger physiological discontinuation attributable to serotonin, potentially allowing for direct switch-overs without the need for tapers or cross-tapers. Few studies have compared switching strategies; we located only one, comparing immediate switching versus 2-week cross-tapering from an SSRI to duloxetine in MDD, revealing no differences in tolerability.¹⁸

An excellent review by Jha et al¹⁹ provides practical suggestions for clinicians in the evaluation and management of suspected antidepressant discontinuation symptoms.

 Protracted or Delayed Symptoms

Anecdotal reports exist of individuals who incur an array of physical symptoms that are either unusually persistent or qualitatively different from traditionally recognized discontinuation symptoms, sometimes emerging many months or even years after actual drug cessation. Based on Naranjo adverse drug reaction criteria,²⁰ it is difficult to establish pharmacodynamic causality with physical complaints long after drug elimination has occurred, barring hypothesized but undemonstrated persistent neuroadaptive changes. Examples of such rare or unusual phenomena include post-SSRI sexual dysfunction²¹ and protracted visual disturbances such as visual snow syndrome.²² Formal literature documenting bona fide instances of unusual somatic phenomena resulting from medication discontinuation is sparse and lacking either in exposure denominators (needed to estimate incidence rates) or matched comparison groups (to identify and control for patient-specific [non-pharmacodynamic] predisposing characteristics).

Delayed-onset “withdrawal,” long after an antidepressant has been eliminated, or protracted/post-acute withdrawal syndrome (“PAWS”), has been described in patients taking an antidepressant continuously for >6 months for whom new and/or more intense symptoms last >6 weeks after drug cessation.^23,24 Published reports derive mainly from self-selected patient internet forums (eg, www.survivingantidepressants.org) without placebo comparisons or formal clinical assessments, reporting a median PAWS duration of 26 months after medication discontinuation following a median 79 months’ treatment duration.²⁵

No known physiological mechanisms plausibly account for pharmacodynamically based “withdrawal” symptoms that arise de novo long after complete drug elimination has occurred. If there exists an occult pharmacological mechanism by which some adverse neuro-maladaptive process could account for delayed discontinuation phenomena, it awaits empirical demonstration. Until then, clinicians might consider the following plausible patient-specific characteristics as evaluable contributors:

• Residual baseline symptoms: Outcomes likely differ for euthymic versus non-euthymic (or subsyndromally symptomatic) patients with MDD or anxiety disorders who stop an antidepressant. Up to 80% of patients with MDD deemed “responders” to an antidepressant manifest residual symptoms, notably fatigue, psychic anxiety, depressed mood, sexual dysfunction, guilt, or insomnia.^26,27 Failure to identify baseline residual symptoms incurs the risk of conflating drug-induced physical discontinuation phenomena with exacerbations of residual baseline symptoms.
• Nocebo phenomena: Pertinent to assessing suspected adverse drug effects is the nocebo effect, ie, the likelihood of adverse physical effects from a pharmacologically inert substance, misattributed to pharmacodynamic causes. Up to two-thirds of MDD patients in clinical trials report adverse effects while taking placebo.²⁸ Nocebo effects are more common among individuals with neuroticism, proneness to catastrophic thinking, and phobic-obsessive traits,^29-31 as well as alexithymia,³² negative expectancy biases, and impaired interoception (ie, over-sensitized perception of aversive sensory experiences).³³ These traits notably overlap with vulnerabilities to depression and anxiety.
  A meta-analysis found that ~17% of patients discontinuing placebo experienced discontinuation symptoms (versus ~31% discontinuing an antidepressant).³  
  However, no empirical studies have yet formally examined possible associations between antidepressant discontinuation phenomena and the above patient characteristics. One of the few randomized antidepressant discontinuation trials examining discontinuation phenomena found that neither trait anxiety nor tapering duration, treatment duration, or drug half-life were significant predictors.⁸

• Somatic symptoms: World Health Organization data indicate that nearly 70% of MDD patients have prominent somatic symptoms (particularly in non-Western cultures),³⁴ in turn associated with increased likelihood of adverse effects during antidepressant trials.^35,36 Patients with MDD plus high somatosensory amplification (the tendency to experience bodily sensations as noxious) tend to attribute more of their general bodily symptoms to medication side effects, suggesting a possible link with antidepressant discontinuation phenomena, and the psychological mechanisms underlying risk for nocebo phenomena. An analogous process may bear on perceived aversive physical experiences when stopping an antidepressant, especially if harm expectancy pre-exists. Clinicians’ explicit warnings of “serious withdrawal risks” may also condition or induce such expectations of an increased likelihood of harm.³⁷
  Further relevant to this concept is the idea of somatization (the process by which psychological distress is expressed as physical symptoms) as a defense mechanism in the setting of innate psychological distress.³⁸ Notably, the DSM-5 diagnosis of somatic symptom disorder (SSD) hinges on distress and disruption to daily functioning caused by physical symptoms (regardless of etiology), with excessive thoughts or behaviors related to those symptoms, lasting >6 months. Clinicians should consider SSD in the differential diagnosis of prolonged antidepressant “discontinuation phenomena.”

• Trauma histories: Trauma may predispose individuals to heightened threat appraisal, thereby increasing symptom vigilance and harm expectancy. Trauma histories are also associated with the development of schema patterns such as mistrust/abuse, abandonment/instability, and emotional deprivation, wherein interactional patterns are predicated on unmet care or dependency needs and fear of harm.³⁹ These schema patterns frequently resonate with interactional styles with clinical caregivers and treatments. Studies are needed to examine potential links between past trauma, harm expectancy bias, and adverse physical experiences from either starting or stopping psychotropic medications.

Summary

Acute antidepressant discontinuation symptoms are well-established and largely pharmacodynamic, whereas mechanistic explanations for persistent or delayed symptoms remain uncertain. Existing studies suggest that discontinuation symptoms likely reflect physiological de-adaptation states that are typically transient, are medically self-limited, and generally do not include relapsing symptoms of the psychiatric condition that was originally being treated (but may signal a risk for future relapse). “Delayed-onset” withdrawal-type symptoms arising long after antidepressant discontinuation are difficult to explain pharmacodynamically and should prompt screening for a relapsing underlying psychiatric condition and/or somatic symptom disorder. Regardless of etiology, somatic symptoms after antidepressant discontinuation can be distressing and foster speculation about protracted physiological withdrawal, enduring brain adaptations to prior medication exposures, and perceived harm. Current evidence does not permit confident attribution of persistent post-discontinuation symptoms to either ongoing neurobiological adaptations or non-pharmacodynamic mechanisms.

Caution must be exercised when evaluating somatic complaints after antidepressant discontinuation, particularly when at variance with commonly observed discontinuation phenomena and their physiologically expected timeframes. Reinstituting a discontinued antidepressant long after its cessation may not necessarily ameliorate these complaints but may warrant consideration in select cases. It is imperative for clinicians to validate patients’ experience of suffering, collaboratively track and monitor complaints, and compassionately explore psychological or other non-pharmacodynamic factors that may lead to the expression of emotional distress via somatic complaints.

Published Online: August 6, 2026. https://doi.org/10.4088/JCP.26ac16648
© 2026 Physicians Postgraduate Press, Inc.

J Clin Psychiatry 2026;87(4):26ac16648

To Cite: Goldberg JF, Crismon ML, Goodman DW, et al. When do physical symptoms after antidepressant cessation reflect pharmacodynamic versus non-pharmacodynamic clinical phenomena? J Clin Psychiatry. 2026;87(4):26ac16648.

Author Affiliations: Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, New York (Goldberg, Ernst); The University of Texas at Austin, College of Pharmacy and Department of Psychiatry, Austin, Texas (Crismon); Johns Hopkins Medical Institutions, Department of Psychiatry, Baltimore, Maryland (Goodman); Department of Psychiatry, SUNY Upstate Medical University, Syracuse, New York (Goodman, Mago); Peter O’Donnell Jr. Brain Institute and the Department of Psychiatry, UT Southwestern Medical Center, Dallas, Texas (Jha); Institute for Mental and Physical Health and Clinical Translation (IMPACT), School of Medicine, Deakin University, The Geelong Clinic and Barwon Health, Geelong, Victoria, Australia (Berk); Orygen The National Centre of Excellence in Youth Mental Health, The Florey Institute of Neuroscience and Mental Health and Department of Psychiatry, University of Melbourne, Melbourne, Australia (Berk); Department of Public Health and Preventative Medicine, Monash University, Melbourne, Australia (Berk); Department of Psychiatry and Behavioral Sciences, New York Medical College, Valhalla, New York (Citrome); Department of Psychiatry and Behavioral Sciences, Northwestern Feinberg School of Medicine, Chicago, Illinois (Citrome); Department of Psychiatry, University of Toronto, Toronto, Ontario, Canada (McIntyre); Department of Pharmacology and Toxicology, University of Toronto, Ontario, Canada (McIntyre); Duke-NUS Medical School, Singapore (Rush); Department of Pharmacotherapy, University of North Texas Health College of Pharmacy; Fort Worth, Texas (Cohen); Touro College of Pharmacy, Touro University, New York, New York (Cohen); Department of Psychiatry and Neurobehavioral Sciences, University of Virginia School of Medicine, Charlottesville, Virginia (Clayton); Department of Psychiatry & Behavioral Sciences, University of New Mexico, Albuquerque, New Mexico (Tohen); Department of Psychiatry and Behavioral Sciences, Kansas University School of Medicine-Wichita, Kansas (Preskorn); Corporal Michael J Cresencz VAMC, Philadelphia, Pennsylvania (Thase); Department of Psychiatry, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania (Thase); University of Pittsburgh, Western Psychiatric Institute and Clinic, Pittsburgh, Pennsylvania (Swartz); Department of Psychiatry, NYU Grossman School of Medicine, New York, New York (Iosifescu); Nathan Kline Institute, Orangeburg, New York (Iosifescu); Department of Obstetrics and Gynecology, College of Medicine, University of Florida, Florida (Roussos-Ross); Department of Psychiatry, College of Medicine, University of Florida, Florida (Roussos-Ross); Department of Psychiatry and Behavioral Sciences, Stanford University, Palo Alto, California (Rapaport).

Corresponding Author: Joseph F. Goldberg, MD, 128 East Avenue, Norwalk, CT 06851 ([email protected]).

Financial Disclosure: Dr Goldberg has been a consultant to Abbvie, Alkermes, Almatica, Alvogen, Compass Pathways, Genomind, Neurelis, Neuroma, Otsuka, Puretech, and Seaport Therapeutics; has received royalties from American Psychiatric Publishing, and Cambridge University Press; and has been on speakers bureaus for Alkermes, Axsome, Bristol Myers Squibb, Intracellular Therapies, Johnson and Johnson, and Vanda Pharmaceuticals. Dr Goodman has served as consultant/faculty to National Football League; World Anti-doping Agency; Expert Advisory Group, National Academies of Sciences, Engineering, and Medicine; American Professional Society of ADHD and Related Disorders (APSARD); Children and Adults with ADHD Association (CHADD); Medscape; Neuroscience Education Institute; HPClive, University of California-Riverside, and University of Cincinnati. Dr Jha has received research contract grants from Neurocrine Bioscience, Navitor/Supernus and Janssen Research & Development; consultant fees from Janssen Scientific Affairs, Neurocrine, AbbVie, Definium/MindMed, Sanofi and Boehringer Ingelheim; fees to serve on Data Safety and Monitoring Board from Worldwide Clinical Trials (Eliem, Skye and Inversargo), Vicore Pharma and IQVIA (Click); and honoraria for educational presentations from North American Center for Continuing Medical Education, Medscape/WebMD, Soterix Medical Inc., Clinical Care Options, Physicians’ Education Resource, Efficient CME, and H.C. Wainwright & Co and to serve as Section Editor of the Psychiatry & Behavioral Health Learning Network and as Guest Editor for Psychiatric Clinics of North America from Elsevier. Dr Berk has received grant/research support from National Health and Medical Research Council, Wellcome Trust, Medical Research Future Fund, Victorian Medical Research Acceleration Fund, Centre for Research Excellence CRE, Victorian Government Department of Jobs, Precincts and Regions, and Victorian COVID-19 Research Fund and has received honoraria from Springer, Oxford University Press, Cambridge University Press, Allen and Unwin, Lundbeck, Controversias Barcelona, Servier, Medisquire, HealthEd, Australian and New Zealand Journal of Psychiatry, EPA, Janssen, Medplan, Milken Institute, Royal Australian and New Zealand College of Psychiatrists, Abbott India, American Society of Clinical Psychopharmacology, Headspace, and Sandoz. Dr Citrome has been a consultant for Abbvie, Acadia, Adheretech, Altus, Alumis, Axsome, Alkermes, Arc, Auritec, Autobahn, Avant Healthcare Solutions, Biogen, BioXcel, BMS/Karuna, Boehringer Ingelheim, Cadent, Cerevel, Clario/Medavante/Prophase, Clinilabs, Compass, Corcept, Definium, Delpor, Eisai, Enteris BioPharma, Health Wellness Partners, HLS, Idorsia, Inmune Bio, Intra-Cellular, Johnson & Johnson/Janssen, Little Bear, Lundbeck, Luye, Lyndra, Maplight, Marvin, Mindmed, Neurelis, Neushen, Neumora, Neurocrine, Noema, Novartis, Noven, Orexo, Otsuka, Ovid, Pontifax/Draig, Praxis, PSL, Real Chemistry, Relmada, Renew Research, Response, Reviva, Sage, Seaport, Sumitomo/Sunovion, Supernus, Teva, University of Arizona, Vanda, and Wells-Fargo and one-off ad hoc consulting for individuals/entities conducting marketing, commercial, or scientific scoping research; has received honoraria for lectures from Abbvie, Acadia, Alkermes, BMS, Eisai, Idorsia, Intra-Cellular, Johnson & Johnson/Janssen, Lundbeck, Luye, Neopharm, Neurocrine, Noven, Otsuka, Recordati, Takeda, Teva, Vanda, and CME activities organized by medical education companies such as Decera Clinical Education/Clinical Education Alliance/Clinical Care Options, CME Institute, CMEology, HMP/Psych Congress, Medscape/WebMD, MultiMedia Medical LLC, Neuroscience Education Institute, NEI, Paradigm, Real Psychiatry/Efficient, Real World; owns health-related stocks as follows: portfolio of small number of shares of common stock of multiple companies and managed externally, stock options: Reviva; and has received royalties/publishing income from Taylor & Francis (Editor-in-Chief, Current Medical Research and Opinion, 2022-date), UpToDate (reviewer), Springer Healthcare (book), Elsevier (Topic Editor, Psychiatry, Clinical Therapeutics, through Spring 2025). Dr McIntyre has received grant support from Canadian Institutes of Health Research/Global Alliance for Chronic Diseases/National Natural Science Foundation of China (NSFC) and the Milken Institute and speaker/consultation fees from Lundbeck, Janssen, Alkermes, Neumora Therapeutics, Boehringer Ingelheim, Sage, Biogen, Mitsubishi Tanabe, Purdue, Pfizer, Otsuka, Takeda, Neurocrine, Neurawell, Sunovion, Bausch Health, Axsome, Novo Nordisk, Kris, Sanofi, Eisai, Intra-Cellular, NewBridge Pharmaceuticals, Viatris, Abbvie, Bristol Myers Squibb (BMS), and Atai Life Sciences. Dr Rush has received royalties from Wolters Kluwer Health, Guilford Press; consulting fees from Beckley Psytech Inc., Better Up Inc., Compass Inc., Emmes Corp., Evecxia Therapeutics, Inc., Holmusk Technologies, Inc., ICON, PLC, Johnson & Johnson (Janssen), Liva Nova; Neurocrine Biosciences Inc., MindStreet, Inc., and Otsuka-US and honoraria from Liva Nova and holds the following patents: US Patent No. 7,795,033: Methods to Predict the Outcome of Treatment with Antidepressant; Medication, Inventors: McMahon FJ, Laje G, Manji H, Rush AJ, Paddock S, Wilson AS; and US Patent No. 7,906,283: Methods to Identify Patients at Risk of Developing Adverse Events During Treatment with Antidepressant Medication, Inventors: McMahon FJ, Laje G, Manji H, Rush AJ, Paddock S. Dr Clayton has received grants from Dare Bioscience, Janssen, Neumora Therapeutics, Neurocrine Biosciences, National Institutes of Health, Relmada Therapeutics, Reunion Neuroscience, S1 Biopharma; royalties from Ballantine Books; Changes in Sexual Functioning Questionnaire; Guilford Publications; and consulting fees from AbbVie, ACCUMIN, Actinogen, AdhereTech, Axsome Therapeutics, Aytu BioPharma; Biogen, Fabre-Kramer, Intracellular Therapies, Janssen R&D, LivaNova, Mycomedica Life Sciences, Neumora Therapeutics, Reunion Neuroscience, s1 Biopharma, Seaport Therapeutics, Sirtsei Pharmaceuticals, Vella Bioscience; and has stock or stock options in Mediflix LLC and S1 Biopharma. Dr Tohen has received consulting fees from Abbvie, Alkermes, Bristol Myers Squibb, Johnson and Johnson, Otsuka, Lundbeck, Minerva, and Teva. Dr Preskorn has received consulting fees from BioXcel Therapeutics, Inc. and Janssen Research and Development, LLC and honoraria from Alkermes. Dr Thase has been an advisor/consultant for Atai-Beckley, Autobahn Therapeutics, Axsome Therapeutics, Bristol Myers Squibb, Clexio Biosciences, Eli Lilly and Co., GH Research, H. Lundbeck, A/S, Johnson and Johnson (includes Intracellular Therapies and Janssen Pharmaceuticals, Merck and Co., Otsuka Pharmaceutical Co., Ltd., and Sage Pharmaceuticals; received grants from Atai Beckley, Johnson & Johnson (includes Intracellular Therapies, Inc. and Janssen Pharmaceuticals, Inc., National Institute of Mental Health; Patient-Centered Outcomes Research Institute; Reunion Pharmaceuticals; and received royalties from American Psychiatric Foundation and Kluwer Wolters, and his spouse is employed by Open Health. Dr Swartz has received royalties from American Psychiatric Publishing, Wolters Kluwer, New Harbinger Publications; consulting fees from Mediflix; and honoraria for lectures from Clinical Education Alliance, Intracellular Therapies, and WebMD/MedScape and participated on a Data Safety Monitoring Board: R01 MH125155 IM Ketamine vs. Midazolam for Suicidal ER Patients. Dr Iosifescu has been a consultant for Alkermes, Allergan, Autobahn, Axsome Therapeutics, Biogen, Boehringer Ingelheim, Centers for Psychiatric Excellence, Clexio, Delix, Jazz, Lundbeck, Neumora, Otsuka, Precision Neuroscience, Relmada, Sage, and Sunovion and has received research funding (through his academic institutions) from Alkermes, Astra Zeneca, Brainsway, Litecure, Neosync, Otsuka, Roche, and Shire. Dr Ernst has received royalties from American Psychiatric Publishing. Dr Rapaport is co-founder of “Renewal Streaming Service.” Drs Crismon, Mago, Cohen, and Roussos-Ross have no financial disclosures to report.

Funding/Support: None.

Acknowledgments: Dr Jha is supported by National Institute of Mental Health grant MH126202, and Dr Berk is supported by a National Health and Medical Research Council Leadership 3 Investigator grant (GNT2017131).

Artificial Intelligence (AI-assisted) Technology: None was used.

Publisher’s Note: The editor of the ASCP Corner, Leslie Citrome, MD, MPH, recused himself from the peer review process. J. Craig Nelson, MD, founding editor of the ASCP Corner, oversaw the peer review process for this manuscript.