What is Acute Stress Disorder?
Acute stress disorder (ASD) is an emotional and psychological reaction to trauma. People develop ASD after experiencing a shocking or frightening event, such as a natural disaster, a car accident, or sexual assault. Some people develop the disorder when they are indirectly exposed to trauma, such as witnessing something traumatic or when a loved one goes through a traumatic event.
Some estimates suggest that as many as a third of people who experience trauma experience symptoms of ASD.
Symptoms of ASD may include:
- Recurring, intrusive, and distressing memories of the trauma
- Distressing dreams about the trauma
- Extreme distress when reminded of the trauma
- Exaggerated reaction to being startled, such as by loud noises or sudden movements
- Memory loss related to the trauma
- Avoidance of reminders and situations associated with the trauma
- Irritability or anger
- Sleep disruption
- Lack of positive emotions
- Problems with concentration
- Feeling numb or in a daze
- Feeling disconnected from yourself or reality
ASD symptoms are similar to those of post-traumatic stress disorder (PTSD). However, ASD differs from PTSD in that its symptoms are temporary and resolve within a month after they begin. By contrast, PTSD is only diagnosable if its symptoms persist for more than a month. People with ASD are also more likely to experience a feeling of disconnection from reality (dissociative symptoms). Some people who are initially diagnosed with ASD are later diagnosed with PTSD.
What Causes Acute Stress Disorder?
ASD typically occurs after a traumatic event or a significant stressor. It’s normal to experience an immediate panicked reaction to a brutal attack, combat injury, or a natural disaster. However, ASD symptoms cause more than typical distress and interfere with a person’s ability to function in their daily life.
People are at an increased risk for developing ASD after experiencing trauma if they have certain risk factors, such as:
- Having experienced other trauma in the past
- Having experienced PTSD in the past
- Having experienced other mental health issues in the past
- Having a history of dissociative symptoms in reaction to trauma
Some studies have shown that the type of trauma experienced affects the risk of developing ASD. For example, accidents and natural disasters are unlikely to cause the disorder, while assaults, violent crimes, and mass shootings are more likely to cause ASD.
Is Acute Stress Disorder Hereditary?
It is not clear whether genes are directly responsible for a person’s risk of developing ASD, but research has identified some apparent genetic predispositions for PTSD that may also be at play in ASD. In 2017, the Psychiatric Genomics Consortium found molecular evidence pointing to genetic risk for PTSD after trauma. In addition, the study showed that the risk of PTSD is strongest among women.
Using a genome-wide association study (GWAS) technique, researchers found that among American women of European descent, genetic factors influenced 29% of the risk for developing PTSD. The genetic risk for PTSD is substantially lower in men.
How Is Acute Stress Disorder Detected?
ASD symptoms typically emerge shortly after a traumatic experience. In many cases, symptoms begin very quickly, sometimes within minutes of the trauma. However, symptoms must last for at least three days to meet the diagnostic criteria for ASD.
Early symptoms of the disorder may be physical signs such as:
- Shortness of breath
- Rapid heartbeat
- Chest pain
- Stomach pain
- Abnormal sweating
Early psychological symptoms may include:
- Problems concentrating or focusing
- Intrusive thoughts
- Low mood
How Is Acute Stress Disorder Diagnosed?
A doctor with experience in diagnosing mental illnesses, such as a psychiatrist or psychologist, can diagnose ASD. To be diagnosed with ASD, a person must have experienced trauma, either directly or indirectly. In addition, they must have at least nine symptoms that last between three days and a month. Symptoms fall into five different categories, including:
- Intrusive symptoms
- Negative mood
- Dissociative symptoms
- Avoidance symptoms
- Arousal symptoms
The symptoms must not be caused by substance use or a medical condition.
PLEASE CONSULT A PHYSICIAN FOR MORE INFORMATION.
How Is Acute Stress Disorder Treated?
People with ASD often respond well to therapy and behavioral changes. Medications are not typically recommended for the treatment of ASD, but some doctors may temporarily prescribe medications to relieve symptoms such as anxiety.
- Cognitive-behavioral therapy (CBT) helps people change their thought patterns by talking about the trauma or unearthing the origins of their fears. CBT is a safe and effective intervention for both acute and chronic PTSD. The therapeutic technique helps individuals integrate their thoughts, feelings, and behaviors.
- Trauma-focused cognitive behavioral therapy (TFCBT) is a specific type of CBT developed to help children, adolescents, adult survivors, and families recover from the damaging effects of trauma.
How Does Acute Stress Disorder Progress?
By definition, ASD is a short-term disorder. Its symptoms resolve within a month. If symptoms persist longer, the diagnosis is likely to be changed to PTSD.
How Is Acute Stress Disorder Prevented?
Studies show that TCBT can be effective when used immediately after someone experiences a traumatic event. The therapy treats the immediate symptoms of ASD and reduces the risk of the disorder evolving into PTSD.
In some cases, the support and attention of loved ones, family members, and counselors in the aftermath of trauma are enough to prevent or relieve the symptoms of ASD.
Acute Stress Disorder Caregiver Tips
The most important thing you can do for a loved one with ASD is be supportive and caring.
- Create a calm, comforting environment.
- Don’t argue with someone who is fearful and hyper-vigilant.
- Be patient with irritability and anger.
- Embrace a daily routine.
- Encourage daily physical activity.
- Avoid situations that trigger flashbacks.
Some people with ASD also suffer from other brain and mental health-related issues, a condition called co-morbidity. Here are a few of the disorders commonly associated with ASD and PTSD:
- Some people with ASD also have an anxiety disorder, including panic disorder, social anxiety disorder, or specific phobias.
- Alcoholism and other substance use disorders are commonly comorbid with PTSD. Substance use may begin as an attempt to self-medicate symptoms, but substance abuse can make symptoms worse.
- The mental disorder most commonly comorbid with PTSD is depression.
Acute Stress Disorder Brain Science
The brain is susceptible to the effects of traumatic stress. Brain scans show that areas of the brain differ significantly in trauma survivors compared to healthy individuals. In the case of PTSD, traumatic stress can be associated with lasting changes in three brain areas. The regions implicated in PTSD include:
- The amygdala, an almond-shaped mass of gray matter, is the brain region that experiences emotions and recognizes them in other people. Trauma activates the amygdala, sparking the body’s fear-response system.
- The hippocampus, a seahorse-shaped structure, is the center of memory, emotions, and motivation. Antidepressant drugs appear to counteract stress by acting on the hippocampus.
- The prefrontal cortex regulates negative emotions such as fear. The ventromedial prefrontal cortex, a region of the brain’s frontal lobe, plays a role in triggering emotions. Severe emotional trauma can cause lasting changes in the prefrontal cortex.
Acute Stress Disorder Research
Title: Intranasal Neuropeptide Y in Clinical Trial in Level Two Trauma Patients for PTSD and Acute Stress Disorder
Stage: Not Yet Recruiting
Principal investigator: Esther Sabban, PhD
New York Medical College
Level 2 trauma patients admitted to Westchester Medical Center who consent and meet the inclusion criteria will answer a questionnaire, be tested on Beck Anxiety Index, be assessed for vital signs, and provide blood and urine samples for biomarker testing before the intervention.
Part 1 Dose Escalation: Subjects will receive a single infusion NPY or vehicle delivered to the upper nasal cavity with an intranasal device. The administration of intranasal NPY will follow the 3 plus 3 model and Fibonacci dose escalation scheme.
Subjects will be assessed for Acute Stress Disorder (ASD) on the National Stressful Events Survey Acute Stress Disorder Sheet (NSESSS) at 3-7 and 14-30 days post-trauma. At >60 days post-trauma, they will be evaluated with the PTSD Symptom Scale Interview for DSM-5 (PSS-I-5) and given the Beck Anxiety Inventory test.
Part 2 Dose Expansion Cohort: Once the maximally tolerated dose (MTD) is determined, we will follow it by a dose expansion cohort to obtain preliminary evidence of the efficacy of intranasal NPY to alter the severity of ASD and inhibit the progression to PTSD and the usefulness of several biomarkers.
Title: Safety & Efficacy of Intranasal Dexmedetomidine, Fentanyl & Midazolam in the Pediatric Emergency Room
Stage: Not Yet Recruiting
Principal investigator: Jonathan Chang, MD
Arkansas Children’s Hospital
Little Rock, AR
Intranasal medications are rapidly gaining popularity as agents for analgesia and anxiolysis in the pediatric hospital setting. One of the primary reasons for the popularity of intranasal medications is the ease of administration combined with favorable pharmacokinetics. It has been well established that children identify venipuncture as one of the most painful and anxiety-producing procedures during time spent in the hospital. These experiences have been shown to have a more lasting impact, producing increased anxiety and fear at subsequent visits. Although oral and rectal administration of analgesics are also non-invasive, bioavailability, time to onset, and half-lives are significantly longer with these routes of administration in comparison to intranasal administration. Multiple studies have shown that intranasal fentanyl, midazolam, and dexmedetomidine have similar pharmacokinetics to intravenous preparations and reach adequate serum levels in both the blood and cerebrospinal fluid. In the pediatric emergency room setting, intranasal fentanyl and midazolam have been shown to provide effective analgesia and anxiolysis for various settings, including pain management (e.g., pain associated with long bone fractures, burns, incision, and drainage) and pre-procedural sedation/anxiolysis (e.g., radiological imaging). Numerous studies have examined the safety and efficacy of intranasal fentanyl and midazolam, and several studies have examined the effectiveness of intranasal dexmedetomidine for non-painful procedural sedation. To date, two studies have compared the use of intranasal dexmedetomidine and intranasal midazolam or intranasal dexmedetomidine, intranasal fentanyl, and intranasal midazolam for anxiolysis in painful procedural sedations. However, as of 2020, no previous studies have compared the use of intranasal dexmedetomidine, intranasal fentanyl, and intranasal midazolam for painful procedures in the pediatric emergency setting.
Title: PTSD Prevention Using Oral Hydrocortisone
Principal investigator: Rachel Yehuda, PhD
Icahn School of Medicine at Mount Sinai
New York, NY
There is currently no evidence-based intervention for individuals exposed to trauma that is designed to aid recovery and prevent the development of post-traumatic stress disorder (PTSD). This randomized control trial proposes to test a one-time prophylactic treatment to prevent symptoms of PTSD and related mental health disturbances and the promotion of resilience using a single dose of hydrocortisone (HCORT) or placebo, administered within six hours of trauma exposure. People at risk for PTSD have demonstrated low cortisol levels before and in the aftermath of traumatic exposures, and lower cortisol levels have also been observed in combat veterans with PTSD. Administering HCORT at the time of trauma would help boost the body’s natural stress recovery systems to facilitate resilience.
Participants who present to the emergency department following trauma exposure and report high distress, panic, anxiety, or dissociation will be invited to participate in this clinical trial. Two hundred twenty trauma survivors will be randomized and recruited at two locations: Mount Sinai Hospital in New York City, US, and a civilian/military hospital in Tel Hashomer, Israel. Trauma survivors will be assessed at 2, 6, 12, and 28 weeks post-treatment. HCORT closely resembles cortisol produced in the adrenal glands and released during stress.
It is hypothesized that HCORT treatment will result in an accelerated decline in the presence and severity of PTSD and related mental health symptoms compared to the placebo group. Blood samples will be collected to analyze potential biomarkers to obtain more information about the mechanisms of action of this intervention. The information obtained will be relevant in determining whether early intervention with a single dose of HCORT, compared to placebo, administered within several hours following trauma exposure, will reduce the risk of developing PTSD in trauma survivors.