Posts tagged PTSD
Articles and news from the latest research reports.
Mini-Strokes May Lead to PTSD
A mini-stroke may not cause lasting physical damage, but it could increase your risk of developing post-traumatic stress disorder (PTSD), a small, new study suggests.
Almost one-third of patients who suffered a mini-stroke — known as a transient ischemic attack (TIA) — developed symptoms of PTSD, including depression, anxiety and reduced quality of life, the researchers said.
"At the moment, a TIA is seen by doctors as a fairly benign disorder," said study co-author Kathrin Utz, a researcher in the department of neurology at the University of Erlangen-Nuremberg in Germany.
In a novel brain-imaging study among trauma victims, researchers at NYU Langone Medical Center have linked an opioid receptor in the brain — associated with emotions — to a narrow cluster of trauma symptoms, including sadness, emotional detachment and listlessness. The study, published online today in the journal JAMA Psychiatry, holds important implications for targeted, personalized treatment of post-traumatic stress disorder, or PTSD, a psychiatric condition affecting more than 8 million Americans that can cause a wide range of debilitating psychiatric symptoms.
“Our study points toward a more personalized treatment approach for people with a specific symptom profile that’s been linked to a particular neurobiological abnormality,” says lead author Alexander Neumeister, MD, director of the molecular imaging program in the Departments of Psychiatry and Radiology at NYU School of Medicine, and Co-Director of NYU Langone’s Steven and Alexandra Cohen Veterans Center for the Study of Post-Traumatic Stress Disorder and Traumatic Brain Injury. “Understanding more about where and how symptoms of PTSD manifest in the brain is a critical part of research efforts to develop more effective medications and treatment modalities.”
The new study confirms a growing body of evidence linking a particular set of symptoms to specific brain circuits and chemicals, and bolsters a shift within the field of psychiatry away from “one-size-fits-all treatments” and toward more individualized medication regimens that target highly specific neurobiological components. “We know from previous clinical trials that antidepressants, for example, do not work well for dysphoria and the numbing symptoms often found in PTSD,” Dr. Neumeister added. “Currently available antidepressants are just not linked specifically enough to the neurobiological basis of these symptoms in PTSD. Going forward, our study will help pave the way toward development of better options.”
“People with cancer have a variety of different treatment options available based on the type of cancer that they have,” adds Dr. Neumeister. “We aim to do the same thing in psychiatry. We’re deconstructing PTSD symptoms, linking them to different brain dysfunction, and then developing treatments that target those symptoms. It’s really a revolutionary step forward that has been supported by the National Institute of Mental Health (NIMH) over the past few years in their Research Domain Criteria Project.”
The study, funded by the National Institute of Mental Health (NIMH), compared the brain scans of healthy volunteers with those of clinically diagnosed trauma victims with PTSD, major depression, and generalized anxiety disorder whose symptoms ranged from emotional detachment to isolation. Participants received a harmless radioactive tracer that binds to and illuminates a class of opioid receptors, known as kappa, when exposed to high-resolution positron emission tomography (PET). Kappa opioid receptors bind a potent natural opioid known as dynorphin, which is released by the body during times of stress to help relieve dysphoria or numbing.
Chronic exposure to stress, such as the case with PTSD, taxes kappa opioid receptors, however, causing the receptors to retract inside cells, leaving dynorphin without a place to dock. As a result, patients can experience dysphoria, characterized by feelings of hopelessness, detachment and emotional unease.
Results showed that fewer available kappa opioid receptors in the brain regions believed to govern emotions were associated with more intense feelings of dysphoria, but not feelings of anxious arousal. The findings confirm previous studies in animals linking the opioid-receptor system expressed in these specific brain regions to symptoms of dysphoria. The study also found an association between lower levels of cortisol, a stress hormone, and unavailable kappa opioid receptors, suggesting a new role for cortisol as a biomarker for certain types of PTSD symptoms.
“This is the first brain-imaging study to explore any psychiatric condition using a protein that binds to the kappa opioid receptor system,” notes Dr. Neumeister, who says the data support clinical trials under way at NYU Langone and other institutions of new medications that target kappa opioid receptors and other brain systems that can be linked to specific symptoms in trauma survivors. Such medications could be widely available for the treatment of PTSD in the future if ongoing clinical trials yield encouraging results.
(Image: Alamy)
EEG Study Findings Reveal How Fear is Processed in the Brain
An estimated 8% of Americans will suffer from post traumatic stress disorder (PTSD) at some point during their lifetime. Brought on by an overwhelming or stressful event or events, PTSD is the result of altered chemistry and physiology of the brain. Understanding how threat is processed in a normal brain versus one altered by PTSD is essential to developing effective interventions.
New research from the Center for BrainHealth at The University of Texas at Dallas published online today in Brain and Cognition illustrates how fear arises in the brain when individuals are exposed to threatening images. This novel study is the first to separate emotion from threat by controlling for the dimension of arousal, the emotional reaction provoked, whether positive or negative, in response to stimuli. Building on previous animal and human research, the study identifies an electrophysiological marker for threat in the brain.
“We are trying to find where thought exists in the mind,” explained John Hart, Jr., M.D., Medical Science Director at the Center for BrainHealth. “We know that groups of neurons firing on and off create a frequency and pattern that tell other areas of the brain what to do. By identifying these rhythms, we can correlate them with a cognitive unit such as fear.”
Utilizing electroencephalography (EEG), Dr. Hart’s research team identified theta and beta wave activity that signifies the brain’s reaction to visually threatening images.
“We have known for a long time that the brain prioritizes threatening information over other cognitive processes,” explained Bambi DeLaRosa, study lead author. “These findings show us how this happens. Theta wave activity starts in the back of the brain, in it’s fear center – the amygdala – and then interacts with brain’s memory center - the hippocampus – before traveling to the frontal lobe where thought processing areas are engaged. At the same time, beta wave activity indicates that the motor cortex is revving up in case the feet need to move to avoid the perceived threat.”
For the study, 26 adults (19 female, 7 male), ages 19-30 were shown 224 randomized images that were either unidentifiably scrambled or real pictures. Real pictures were separated into two categories: threatening (weapons, combat, nature or animals) and non-threatening (pleasant situations, food, nature or animals).
While wearing an EEG cap, participants were asked to push a button with their right index finger for real items and another button with their right middle finger for nonreal/scrambled items. Shorter response times were recorded for scrambled images than the real images. There was no difference in reaction time for threatening versus non-threatening images.
EEG results revealed that threatening images evoked an early increase in theta activity in the occipital lobe (the area in the brain where visual information is processed), followed by a later increase in theta power in the frontal lobe (where higher mental functions such as thinking, decision-making, and planning occur). A left lateralized desynchronization of the beta band, the wave pattern associated with motor behavior (like the impulse to run), also consistently appeared in the threatening condition.
This study will serve as a foundation for future work that will explore normal versus abnormal fear associated with an object in other atypical populations including individuals with PTSD.
Yogic breathing shows promise in reducing symptoms of post-traumatic stress disorder
One of the greatest casualties of war is its lasting effect on the minds of soldiers. This presents a daunting public health problem: More than 20 percent of veterans returning from the wars in Iraq and Afghanistan have post-traumatic stress disorder, according to a 2012 report by RAND Corp.
A new study from the Center for Investigating Healthy Minds at the Waisman Center of the University of Wisconsin-Madison offers hope for those suffering from the disorder. Researchers there have shown that a breathing-based meditation practice called Sudarshan Kriya Yoga can be an effective treatment for PTSD.
Individuals with PTSD suffer from intrusive memories, heightened anxiety, and personality changes. The hallmark of the disorder is hyperarousal, which can be defined as overreacting to innocuous stimuli, and is often described as feeling “jumpy,” or easily startled and constantly on guard.
Hyperarousal is one aspect of the autonomic nervous system, the system that controls the beating of the heart and other body functions, and governs one’s ability to respond to his or her environment. Scientists believe hyperarousal is at the core of PTSD and the driving force behind some of its symptoms.
Standard treatment interventions for PTSD offer mixed results. Some individuals are prescribed antidepressants and do well while others do not; others are treated with psychotherapy and still experience residual affects of the disorder.
Sudarshan Kriya Yoga is a practice of controlled breathing that directly affects the autonomic nervous system. While the practice has proven effective in balancing the autonomic nervous system and reducing symptoms of PTSD in tsunami survivors, it has not been well studied until now.
The CIHM team was interested in Sudarshan Yoga because of its focus on manipulating the breath, and how that in turn may have consequences for the autonomic nervous system and specifically, hyperarousal. Theirs is the first randomized, controlled, longitudinal study to show that the practice of controlled breathing can benefit people with PTSD.
"This was a preliminary attempt to begin to gather some information on whether this practice of yogic breathing actually reduces symptoms of PTSD," says Richard J. Davidson, founder of CIHM and one of the authors of the study. "Secondly, we wanted to find out whether the reduction in symptoms was associated with biological measures that may be important in hyperarousal."
These tests included measuring eye-blink startle magnitude and respiration rates in response to stimuli such as a noise burst in the laboratory. Respiration is one of the functions controlled by the autonomic nervous system; the eye-blink startle rate is an involuntary response that can be used to measure one component of hyperarousal. These two measurements reflect aspects of mental health because they affect how an individual regulates emotion.
The CIHM study included 21 soldiers: an active group of 11 and a control group of 10. Those who received the one-week training in yogic breathing showed lower anxiety, reduced respiration rates and fewer PTSD symptoms.
Davidson would like to further the research by including more participants, with the end goal of enabling physicians to prescribe treatment based on the cognitive and emotional style of the individual patient.
"A clinician could use a ‘tool box’ of psychological assessments to determine the cognitive and emotional style of the patient, and thereby determine a treatment that would be most effective for that individual," he says. "Right now, a large fraction of individuals who are given any one type of therapy are not improving on that therapy. The only way we can improve that is if we determine which kinds of people will benefit most from different types of treatments."
That assessment is critical. At least 22 veterans take their own lives every day, according to the U.S. Department of Veterans Affairs. Because Sudarshan Kriya Yoga has already been shown to increase optimism in college students, and reduce stress and anxiety in people suffering from depression, it may be an effective way to decrease suffering and, quite possibly, the incidence of suicide among veterans.
The study, published in the Journal of Traumatic Stress, was funded by a grant from the Disabled Veterans of America Charitable Service Trust and individual donors.
(Source: news.wisc.edu)
Xenon Exposure Shown to Erase Traumatic Memories
McLean Hospital researchers are reporting that xenon gas, used in humans for anesthesia and diagnostic imaging, has the potential to be a treatment for post-traumatic stress disorder (PTSD) and other memory-related disorders.
“In our study, we found that xenon gas has the capability of reducing memories of traumatic events,” said Edward G. Meloni, PhD, assistant psychologist at McLean Hospital and an assistant professor of Psychiatry at Harvard Medical School. “It’s an exciting breakthrough, as this has the potential to be a new treatment for individuals suffering from PTSD.”
In the study, published in the current issue of PLOS ONE, Meloni, and Marc J. Kaufman, PhD, director of the McLean Hospital Translational Imaging Laboratory, examined whether a low concentration of xenon gas could interfere with a process called reconsolidation – a state in which reactivated memories become susceptible to modification. “We know from previous research that each time an emotional memory is recalled, the brain actually restores it as if it were a new memory. With this knowledge, we decided to see whether we could alter the process by introducing xenon gas immediately after a fear memory was reactivated,” explained Meloni.
The investigators used an animal model of PTSD called fear-conditioning to train rats to be afraid of environmental cues that were paired with brief footshocks. Reactivating the fearful memory was done by exposing the rats to those same cues and measuring their freezing response as a readout of fear. “We found that a single exposure to the gas, which is known to block NMDA receptors involved in memory formation in the brain, dramatically and persistently reduced fear responses for up to 2 weeks. It was as though the animals no longer remembered to be afraid of those cues”, said Dr. Meloni.
Meloni points out that the inherent properties of a gas such as xenon make it especially attractive for targeting dynamic processes such as memory reconsolidation. “Unlike other drugs or medications that may also block NMDA receptors involved in memory, xenon gets in and out of the brain very quickly. This suggests that xenon could be given at the exact time the memory is reactivated, and for a limited amount of time, which may be key features for any potential therapy used in humans.”
“The fact that we were able to inhibit remembering of a traumatic memory with xenon is very promising because it is currently used in humans for other purposes, and thus it could be repurposed to treat PTSD,” added Kaufman.
For these investigators, several questions remain to be addressed with further testing. “From here we want to explore whether lower xenon doses or shorter exposure times would also block memory reconsolidation and the expression of fear. We’d also like to know if xenon is as effective at reducing traumatic memories from past events, so-called remote memories, versus the newly formed ones we tested in our study”.
Meloni and Kaufman indicate that future studies are planned to test if the effects of xenon in rats seen in their study translate to humans. Given that intrusive re-experiencing of traumatic memories – including flashbacks, nightmares, and distress and physiological reactions induced when confronted with trauma reminders – is a hallmark symptom for many who suffer from PTSD, a treatment that alleviates the impact of those painful memories could provide welcome relief.
(Source: mcleanhospital.org)
Passengers who survived terrifying Air Transat flight in 2001, help psychologists uncover new clues about post-traumatic stress vulnerability
An extraordinary opportunity to study memory and post-traumatic stress disorder (PTSD) in a group of Air Transat passengers who experienced 30 minutes of unimaginable terror over the Atlantic Ocean in 2001 has resulted in the discovery of a potential risk factor that may help predict who is most vulnerable to PTSD.
The study, led by researchers at Baycrest Health Sciences, is published online this week in the journal Clinical Psychological Science – ahead of print publication. It is the first to involve detailed interviews and psychological testing in individuals exposed to the same life-threatening traumatic event. By necessity, other trauma studies involve heterogeneous events as experienced in different situations.
This opportunity was enhanced by the fact that one of the researchers, Dr. Margaret McKinnon, was a passenger on the plane. Heading off on her honeymoon in late August 2001, Dr. McKinnon’s flight departed Toronto for Lisbon, Portugal with 306 passengers and crew on board. Mid way over the Atlantic Ocean, the plane suddenly ran out of fuel. Everyone onboard was instructed to prepare for an ocean ditching, which included a countdown to impact, loss of on-board lighting and cabin de-pressurization. About 25 minutes into the emergency, the pilot located a small island military base in the Azores and glided the aircraft to a rough landing with no loss of life and few injuries.
“Imagine your worst nightmare – that’s what it was like,” said Dr. McKinnon, who initiated the study as a postdoctoral fellow at Baycrest’s Rotman Research Institute. She is now a clinician-scientist at St. Joseph’s Healthcare Hamilton and Associate Co-Chair of Research in the Department of Psychiatry and Behavioural Neurosciences at McMaster University in Hamilton.
“This wasn’t just a close call where your life flashes before your eyes in a split second and then everything is okay,” she said. The sickening feeling of “I’m going to die” lasted an excruciating 30 minutes as the plane’s systems shut down.
Following this incident, Dr. McKinnon and her colleagues at Baycrest – including Dr. Daniela Palombo (now a postdoctoral researcher at VA Boston Healthcare System and Boston University School of Medicine) and Dr. Brian Levine (senior scientist at Baycrest’s Rotman Research Institute and the University of Toronto) – recruited 15 passengers to participate in the Baycrest study. Using their knowledge of the moment-to-moment unfolding of events in this disaster, the researchers were able to probe both the quality and accuracy of passengers’ memories for the AT emergency in great detail along with two other events (Sept. 11, 2001 and a neutral event from the same time period) – and relate their findings to the presence or absence of PTSD in those passengers.
Not all passengers on Flight 236 went on to develop PTSD despite experiencing the same “single blow” traumatic event with the threat of imminent death.
The study produced two key findings. First, the Flight 236 passengers showed tremendously enhanced vivid memories of the plane emergency. Although the Baycrest team was not surprised by this, other research has suggested that memory for traumatic events is impoverished. Second, neither the vividness nor accuracy of memory related to who developed PTSD, but those with PTSD recalled a higher number of details external to the main event (i.e. details that were not specific in time, or were repetitions or editorial statements) compared to passengers who did not have PTSD and to healthy controls. This pattern was observed across all events tested, not just the traumatic event, suggesting that it is not just memory for the trauma itself that is related to PTSD, but rather how a person processes memory for events in general.
“What our findings show is that it is not what happened but to whom it happened that may determine subsequent onset of PTSD,” said Dr. Levine, senior author of the study.
This inability to shut out external or semantic details when recalling personally-experienced memories is related to mental control over memory recall, adding to a growing body of evidence that altered memory processing may be a vulnerability factor for PTSD.
A second study, in preparation for publication, involves functional brain imaging of 10 of the passengers from Air Transat Flight 236. The aim is to illuminate the brain mechanisms associated with exposure to this traumatic event.
(Source: baycrest.org)
Biomarker Could Reveal Why Some Develop Post-Traumatic Stress Disorder
Blood expression levels of genes targeted by the stress hormones called glucocorticoids could be a physical measure, or biomarker, of risk for developing Post-Traumatic Stress Disorder (PTSD), according to a study conducted in rats by researchers at the Icahn School of Medicine at Mount Sinai and published August 11 in Proceedings of the National Academy of Sciences (PNAS). That also makes the steroid hormones’ receptor, the glucocorticoid receptor, a potential target for new drugs.
Post-Traumatic Stress Disorder (PTSD) is triggered by a terrifying event, either witnessed or experienced. Symptoms may include flashbacks, nightmares and severe anxiety, as well as uncontrollable thoughts about the event. Not everyone who experiences trauma develops PTSD, which is why the study aimed to identify biomarkers that could better measure each person’s vulnerability to the disorder.
“Our aim was to determine which genes are differentially expressed in relation to PTSD,” said lead investigator Rachel Yehuda, PhD, Professor of Psychiatry and Neuroscience and Director of the Traumatic Stress Studies Division at the Icahn School of Medicine at Mount Sinai. “We found that most of the genes and pathways that are different in PTSD-like animals compared to resilient animals are related to the glucocorticoid receptor, which suggests we might have identified a therapeutic target for treatment of PTSD,” said Dr. Yehuda, who also heads the Mental Health Patient Care Center and PTSD Research Program at the James J. Peters Veterans Affairs Medical Center in the Bronx.
The research team exposed a group of male and female rats to litter soiled by cat urine, a predatory scent that mimics a life-threatening situation. Most PTSD studies until now have used only male rats. Mount Sinai researchers included female rats in this study since women are more vulnerable than men to developing PTSD. The rats were then categorized based on their behavior one week after exposure to the scent. The authors also examined patterns of gene expression in the blood and in stress-responsive brain regions.
After one week of being exposed to soiled cat litter for 10 minutes, vulnerable rats exhibited higher anxiety and hyperarousal, and showed altered glucocorticoid receptor signaling in all tissues compared with resilient rats. Moreover, some rats were treated with a hormone that activates the glucocorticoid receptor called corticosterone one hour after exposure to the cat urine scent. These rats showed lower levels of anxiety and arousal one week later compared with untreated, trauma-exposed rats.
“PTSD is not just a disorder that affects the brain,” said co-investigator Nikolaos Daskalakis, MD, PhD, Associate Research Scientist in the Department of Psychiatry at the Icahn School of Medicine at Mount Sinai. “It involves the entire body, which is why identifying common regulators is key. The glucocorticoid receptor is the one common regulator that consistently stood out.”
(Image: photos.com)
Treating Mental Illness by Changing Memories of Things Past
In the novel À larecherche du temps perdu (translated into English as Remembrance of Things Past), Marcel Proust makes a compelling case that our identities and decisions are shaped in profound and ongoing ways by our memories.
This truth is powerfully reflected in mental illnesses,like post traumatic stress disorder (PTSD) and addictions. In PTSD, memories of traumas intrude vividly upon consciousness, causing distress, driving people to avoid reminders of their traumas, and increasing risk for addiction and suicide. In addiction, memories of drug use influence reactions to drug-related cues and motivate compulsive drug use.
What if one could change these dysfunctional memories? Although we all like to believe that our memories are reliable and permanent, it turns out that memories may indeed be plastic.
The process for modifying memories, depicted in the graphic, is called memory reconsolidation. After memories are formed and stored, subsequent retrieval may make them unstable. In other words, when a memory is activated, it also becomes open to revision and reconsolidation in a new form.
"Memory reconsolidation is probably among the most exciting phenomena in cognitive neuroscience today. It assumes that memories may be modified once they are retrieved which may give us the great opportunity to change seemingly robust, unwanted memories," explains Dr. Lars Schwabe of Ruhr-University Bochum in Germany. He and his colleagues have authored a review paper on the topic, published in the current issue of Biological Psychiatry.
The idea of memory reconsolidation was initially discovered and demonstrated in rodents.
The first evidence of reconsolidation in humans was reported in a study in 2003, and the findings have since continued to accumulate. The current report summarizes the most recent findings on memory reconsolidation in humans and poses additional questions that must be answered by future studies.
"Reconsolidation appears to be a fundamental process underlying cognitive and behavioral therapies. Identifying its roles and mechanisms is an important step forward to fully harnessing the reconsolidation process in psychotherapy," said Dr. John Krystal, Editor of Biological Psychiatry.
The translation of the animal data to humans is a vital step for the potential application of memory reconsolidation in the context of mental disorders. Memory reconsolidation could open the door to novel treatment approaches for disorders such as PTSD or drug addiction.
Notch Developmental Pathway Regulates Fear Memory Formation
Nature is thrifty. The same signals that embryonic cells use to decide whether to become nerves, skin or bone come into play again when adult animals are learning whether to become afraid.
Researchers at Yerkes National Primate Research Center, Emory University, have learned that the molecule Notch, critical in many processes during embryonic development, is also involved in fear memory formation. Understanding fear memory formation is critical to developing more effective treatments and preventions for anxiety disorders such as post-traumatic stress disorder (PTSD). The results are scheduled for publication online this week by the journal Neuron.
"We are finding that developmental pathways that appear to be quiescent during adulthood are transiently reactivated to allow new memory formation to occur," says Kerry Ressler, MD, PhD, professor of psychiatry and behavioral sciences at Emory University School of Medicine and Yerkes National Primate Research Center, and senior author of the paper.
The first author of the paper is postdoctoral fellow Brian Dias, PhD, and co-authors include undergraduates Jared Goodman, Ranbir Ahluwalia and Audrey Easton, and post-doctoral researcher Raul Andero, PhD.
The Notch signaling pathway, present in insects, worms and vertebrates, is involved in embryonic patterning as well as nervous system and cardiovascular development. It’s a way for cells to communicate and coordinate which cells are going to become what types of tissues.
Dias and Ressler probed the Notch pathway because they were examining many genes that are activated in the brains of mice after they learn to become afraid of a sound paired with a mild foot-shock. They were looking for changes in the amygdala, a region of the brain known to regulate fear learning.
The researchers were particularly interested in micro RNAs. MicroRNAs do not encode proteins but can inhibit other genes, often several at once in a coordinated way. Dias and Ressler found that levels of miRNA-34a are increased in the amygdala after fear learning occurs. A day after fear training, animals whose brains were injected with a virus engineered to carry a “sponge” against miRNA-34a froze less often than control animals.
The researchers found that miRNA-34a regulated several genes that encode components of the Notch pathway. They believe their study is the first to link miRNA-34a and Notch signaling to a role in memory consolidation.
Notch is under investigation as a target in the treatment of various cancers and some drugs that target Notch have been well-tolerated by humans.
"From a therapeutic perspective, our data suggest that relevant drugs that regulate Notch signaling could potentially be a starting point for preventing or treating PTSD," Dias says.
(Source: yerkes.emory.edu)
Researcher shows how stress hormones promote brain’s building of negative memories
When a person experiences a devastating loss or tragic event, why does every detail seem burned into memory whereas a host of positive experiences simply fade away?
It’s a bit more complicated than scientists originally thought, according to a study recently published in the journal Neuroscience by ASU researcher Sabrina Segal.
When people experience a traumatic event, the body releases two major stress hormones: norepinephrine and cortisol. Norepinephrine boosts heart rate and controls the fight-or-flight response, commonly rising when individuals feel threatened or experience highly emotional reactions. It is chemically similar to the hormone epinephrine – better known as adrenaline.
In the brain, norepinephrine in turn functions as a powerful neurotransmitter or chemical messenger that can enhance memory.
Research on cortisol has demonstrated that this hormone can also have a powerful effect on strengthening memories. However, studies in humans up until now have been inconclusive – with cortisol sometimes enhancing memory, while at other times having no effect.
A key factor in whether cortisol has an effect on strengthening certain memories may rely on activation of norepinephrine during learning, a finding previously reported in studies with rats.
In her study, Segal, an assistant research professor at the Institute for Interdisciplinary Salivary Bioscience Research at ASU, and her colleagues at the University of California-Irvine showed that human memory enhancement functions in a similar way.
Conducted in the laboratory of Larry Cahill at U.C. Irvine, Segal’s study included 39 women who viewed 144 images from the International Affective Picture Set. This set is a standardized picture set used by researchers to elicit a range of responses, from neutral to strong emotional reactions, upon view.
Segal and her colleagues gave each of the study’s subjects either a dose of hydrocortisone – to simulate stress – or a placebo just prior to viewing the picture set. Each woman then rated her feelings at the time she was viewing the image, in addition to giving saliva samples before and after. One week later, a surprise recall test was administered.
What Segal’s team found was that “negative experiences are more readily remembered when an event is traumatic enough to release cortisol after the event, and only if norepinephrine is released during or shortly after the event.”
“This study provides a key component to better understanding how traumatic memories may be strengthened in women,” Segal added, “because it suggests that if we can lower norepinephrine levels immediately following a traumatic event, we may be able to prevent this memory enhancing mechanism from occurring, regardless of how much cortisol is released following a traumatic event.”
Further studies are needed to explore to what extent the relationship between these two stress hormones differ depending on whether you are male or female, particularly because women are twice as likely to develop disorders from stress and trauma that affect memory, such as in Posttraumatic Stress Disorder (PTSD). In the meantime, the team’s findings are a first step toward a better understanding of neurobiological mechanisms that underlie traumatic disorders, such as PTSD.
(Image: Wikimedia Commons)