High dose hydrocortisone immediately after trauma may alter the trajectory of PTSD: Interplay between clinical and animal studies
Abstract
High-dose corticosteroids have been reported to reduce symptoms of acute stress and post-traumatic stress in polytrauma patients and in animal studies. The underlying mechanism of action remains largely unclear. These issues were addressed in parallel in the clinical and preclinical studies below. In this preliminary study, 25 patients with acute stress symptoms were administered a single intravenous bolus of high-dose hydrocortisone (100-140 mg) or placebo within 6 h of a traumatic event in a prospective, randomized, double-blind, placebo-controlled pilot study. Early single high-dose hydrocortisone intervention attenuated the core symptoms of both the acute stress and of subsequent PTSD in patients. High-dose hydrocortisone treatment given in the first few hours after a traumatic experience was associated with significant favorable changes in the trajectory of exposure to trauma, as expressed by the reduced risk of the development of PTSD post-trauma. In parallel, a comparative study of morphological arborization in dentate gyrus and its modulating molecules was performed in stress-exposed animals treated with high-dose hydrocortisone. Steroid-treated stressed animals displayed significantly increased dendritic growth and spine density, with increased levels of brain-derived neurotrophic factor (BDNF) and obtunded postsynaptic density-95 (PSD-95) levels. The animal study provided insights into the potential mechanism of this intervention, as it identified relevant morphological and biochemical associations to the clinical observations. Thus, evidence from clinical and animal studies suggests that there is a "window of opportunity" in the early aftermath of trauma to help those who are vulnerable to the development of chronic PTSD.
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Previously, hydrocortisone and prolonged exposure initiated within 12 hours posttrauma in ED patients, and brief cognitive behavioral therapy within the first weeks posttrauma in patients with acute stress disorder, were found to reduce subsequent PTSD symptom severity.
“Previously, hydrocortisone (4,5) and prolonged exposure (3) initiated within 12 hours posttrauma in ED patients, and brief cognitive behavioral therapy within the first weeks posttrauma in patients with acute stress disorder (6), were found to reduce subsequent PTSD symptom severity.”
From Intranasal Oxytocin to Prevent Posttraumatic Stress Disorder Symptoms: A Randomized Controlled Trial in Emergency Department Patients (2017) · cites this paper as [5]
All previous findings of effective PTSD prevention were observed in participants with increased risk for PTSD.
“All previous findings of effective PTSD prevention were observed in participants with increased risk for PTSD [i.e., caused by perceived life-threat (3), peritraumatic dissociation (4), or subthreshold acute stress disorder (5,6)].”
From Intranasal Oxytocin to Prevent Posttraumatic Stress Disorder Symptoms: A Randomized Controlled Trial in Emergency Department Patients (2017) · cites this paper as [5]
A single bolus of high dose hydrocortisone in trauma-exposed individuals at an Emergency Department resulted in fewer PTSD symptoms at 2 weeks and 3 months post-trauma relative to placebo.
“In a small sample of participants Zohar et al. [15] recently showed that a single bolus of high dose hydrocortisone in trauma-exposed individuals at an Emergency Department (ED) resulted in fewer PTSD symptoms at 2 weeks and 3 months post-trauma relative to those who received placebo.”
From Efficacy of oxytocin administration early after psychotrauma in preventing the development of PTSD: study protocol of a randomized controlled trial (2014) · cites this paper as [15]
Starting intranasal oxytocin treatment at the latest at day 10 post-trauma is considerably later than hydrocortisone within the first 12 hours post-trauma, the only pharmacological intervention that has currently yielded promising preventive effects.
“In addition, starting intranasal oxytocin treatments at the latest at day 10 post-trauma is considerably later than the timing of the only pharmacological intervention that has currently yielded promising preventive effects, i.e. hydrocortisone within the first 12 hours post-trauma [15,16].”
From Efficacy of oxytocin administration early after psychotrauma in preventing the development of PTSD: study protocol of a randomized controlled trial (2014) · cites this paper as [15]
Recruiting emergency department patients for research purposes early after trauma exposure is feasible, based on previous early intervention studies.
“Based on previous early intervention studies, recruiting ED patients for research purposes early after trauma exposures is feasible [10,15,16,60,98].”
From Efficacy of oxytocin administration early after psychotrauma in preventing the development of PTSD: study protocol of a randomized controlled trial (2014) · cites this paper as [15]
Data on human PTSD support a protective role for adequate glucocorticoid levels at the time of trauma.
“Data on human PTSD support a protective role for adequate glucocorticoid levels at time of trauma.”
From Neurobiological and Systemic Effects of Chronic Stress (2017) · cites this paper as [34]
There is pilot evidence that administration of hydrocortisone shortly after trauma limits subsequent PTSD symptoms in humans.
“There is pilot evidence that this procedure also limits subsequent PTSD symptoms following trauma in humans 75 .”
From Post‐traumatic stress disorder: a state‐of‐the‐art review of evidence and challenges (2019) · cites this paper as [75]
A preliminary study found that administration of cortisol within hours of trauma exposure is more efficacious than placebo in limiting subsequent PTSD.
“Indeed, a preliminary study found that the administration of cortisol within hours of trauma exposure is more efficacious that placebo in limiting subsequent PTSD 75 .”
From Post‐traumatic stress disorder: a state‐of‐the‐art review of evidence and challenges (2019) · cites this paper as [75]
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- Authors
- Zohar, J., Yahalom, H., Kozlovsky, N., Cwikel-Hamzany, S., Matar, M. A., Kaplan, Z., Yehuda, R., & Cohen, H.
- Affiliations
- Tel Aviv University (IL)
- Ben-Gurion University of the Negev (IL)
- Icahn School of Medicine at Mount Sinai (US)
- Corresponding author
- Cohen, Hagit
- Venue
- European Neuropsychopharmacology
- Publisher
- Elsevier BV
- Published
- 2011-11
- Volume
- 21
- Issue
- 11
- Pages
- 796-809
- ISSN
- 0924-977X (ISSN-L)
- OpenAlex
- W2100561031
- Cited by
- 292
- References
- 62
- Citations by year
- 2026: 8 · 2025: 10 · 2024: 9 · 2023: 11 · 2022: 21 · 2021: 18 · 2020: 20 · 2019: 19 · 2018: 20 · 2017: 23 · 2016: 33 · 2015: 27 · 2014: 33 · 2013: 25 · 2012: 11
- FWCI
- 24.84
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- European Neuropsychopharmacology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Social Sciences › Psychology › Clinical Psychology › Posttraumatic Stress Disorder Research
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Social Sciences › Psychology › Clinical Psychology › Child Abuse and Trauma
- Keywords
- cortisol, high-dose corticosteroids, post-traumatic stress disorder, acute stress, polytrauma, spine density, brain-derived neurotrophic factor, PSD-95, stress exposure, window of opportunity
- MeSH terms
- Disks Large Homolog 4 Protein, Acoustic Stimulation, Adult, Analysis of Variance, Animals, Anti-Inflammatory Agents, Anxiety, Brain, Disease Models, Animal, Dose-Response Relationship, Drug, Double-Blind Method, Female, Follow-Up Studies, Gene Expression Regulation, Humans, Hydrocortisone, Male, Membrane Proteins, Middle Aged, Neurons, Pain Measurement, Reflex, Startle, Stress Disorders, Post-Traumatic, Stress, Psychological, Time Factors, Wounds and Injuries, Trauma Severity Indices, Silver Staining, Treatment Outcome, Rats, Sprague-Dawley, Maze Learning, Brain-Derived Neurotrophic Factor, Intracellular Signaling Peptides and Proteins, Dendritic Spines, Rats, Young Adult
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