Posts tagged PTSD
Articles and news from the latest research reports.
What are the risks of post-traumatic stress disorder after an accident?
Many patients continue to suffer from symptoms (headaches, pain) several months after an accident, which can pose a real handicap to their lives. The team of Emmanuel Lagarde, research director at Inserm’s Research Centre for Epidemiology and Biostatistics (Inserm/University of Bordeaux) has studied the subsequent development of 1,300 people who were admitted to A&R between 2007 and 2009 for trauma. The researchers demonstrate that it is possible to identify people who will develop post-traumatic stress disorder, which generally occurs when the individual’s life was put in danger. This will enable their care to be adjusted accordingly. Their work also reveals that post-concussion syndrome, which has wrongly been defined as the consequence of cranial trauma, is only one part of post-traumatic stress disorder.
The results of the study have been published in the journal JAMA Psychiatry.
Every year, one in ten people in France are taken to A&E with a trauma following an accident. The large majority of the victims have only mild injuries and are discharged from hospital quickly. However, a number of them continue to suffer long after their direct injuries have healed. They may, for example, have headaches, uncontrollable fear or maladies of various kinds, vision problems, balancing problems or be irritable. When the symptoms occur simultaneously in a single context, they constitute what is called a syndrome.
Following a trauma, two syndromes are described: post-concussion syndrome (PCS), which occurs after a mild cranial trauma, and post-traumatic stress disorder (PTSD), which is encountered in people who have been exposed to a stressful situation wherein their life, or that of another person, was put in danger. Post-traumatic stress disorder was initially described in soldiers who, after exposure to combat or an explosion, complain of nightmares or obsessive thoughts which they are unable to get rid of. The two syndromes have been described for several years in the successive editions of the Diagnostic and Statistical Manual of Mental Disorders (DSM) of the American Psychiatric Association, which is a current standard reference in the area of diagnosis in mental health.
In this study, 1,300 people who were admitted to A&E at the Bordeaux Hospital Centre between 2007 and 2009 were contacted three months after their accident. Over 500 were suffering from a mild cranial trauma when they were admitted to hospital while the others had various injuries, all either mild or moderate in severity. The researchers measured the occurrence of 36 symptoms which are included in the definitions of PCS and PTSD.
‘Post-concussion syndrome (PCS) does not deserve its name because, on the one hand, the symptoms that constitute it are not specific to cranial trauma and, on the other, they do not occur simultaneously. It seems that PCS is, in reality, only one part of post-traumatic stress disorder’, explained Emmanuel Lagarde, research director at Inserm.
Post-traumatic stress disorder in the general population
The results obtained also make it possible to have a better understanding of post-traumatic stress disorder, which is still insufficiently described for non-military contexts. In the general population, this disorder occurs in 2% of injured people but this figure rises to 9% when the trauma is cranial. However, it is more frequent among women and people who have been in a road accident or have been attacked. The occurrence of PTSD is also influenced by the state of the victim’s physical and mental health before the accident. All this information can enable doctors to determine if early treatment should be provided.
This study puts the classification of post-traumatic complaints into question because it also questions the very existence of post-concussion syndrome, which should be seen as only one part of post-traumatic stress disorder. These results do not, however, question the reality of the suffering of a significant number of people affected by this disorder, for whom the symptoms continue to persist and considerably impact the quality of their lives.
‘This is why it is necessary to describe these syndromes and their origin more accurately, particularly because identifying them also has important consequences in terms of insurance, compensation and the care and rehabilitation policies of patients’, stressed Emmanuel Lagarde, who is the main author of this work.
Brain responses to emotional images predict PTSD symptoms after Boston Marathon bombing
The area of the brain that plays a primary role in emotional learning and the acquisition of fear – the amygdala – may hold the key to who is most vulnerable to post-traumatic stress disorder.
Researchers at the University of Washington, Boston Children’s Hospital, Harvard Medical School and Boston University collaborated on a unique opportunity to study whether patterns of brain activity predict teenagers’ response to a terrorist attack.
The team had already performed brain scans on Boston-area adolescents for a study on childhood trauma. Then in April 2013 two bombs went off at the finish line of the Boston Marathon, killing three people and injuring hundreds more. Even people who were nowhere near the bombing reported distress about the attack and the days-long manhunt for the suspects.
So, one month after the attack, Katie McLaughlin, then at Boston Children’s Hospital and Harvard Medical School and now an assistant professor of psychology at the UW; co-author Margaret Sheridan, of Boston Children’s Hospital and Harvard Medical School; and their fellow researchers sent online surveys to teenagers who had previously participated in studies to assess PTSD symptoms related to the attack.
By using functional Magnetic Resonance Imaging scans from before the attack and survey data from after, the researchers found that heightened amygdala reaction to negative emotional stimuli was a risk factor for later developing symptoms of PTSD.
The research study was published July 3 in the journal Depression and Anxiety.
“The amygdala responds to both negative and positive stimuli, but it’s particularly attuned to identifying potential threats in the environment,” said McLaughlin, the study’s first author. “In the current study of adolescents the more their amygdala responded to negative images, the more likely they were to have symptoms of PTSD following the terrorist attacks.”
The brain scans were conducted during the year prior to the bombing. At that time, the teens were evaluated for their responses to emotional stimuli by viewing neutral and negative images. Neutral images included items such as a chair or button. Negative images showed people who were sad, fighting or threatening someone else. Participants rated the degree of emotion they felt while looking at each image. The MRIs measured whether blood flow increased to the amygdala and the hippocampus when viewing negative images as compared to neutral images.
In the follow-up survey the teens were asked whether they were at the finish line during the bombing, how much media exposure they had after the attack, whether they were part of the lockdown at home or school while authorities searched for the suspects, and how their parents responded to the incident. They also were asked about specific PTSD symptoms, such as how often they had trouble concentrating and whether they kept thinking about the bombing when they tried not to.
Researchers found a significant association between amygdala activation while viewing negative images and whether the teens developed PTSD symptoms after the bombing.
McLaughlin said a number of previous studies have shown that people with PTSD had heightened amygdala responses to negative emotions, but researchers didn’t know whether that came before or after the trauma.
“It’s often really difficult to collect neurobiological markers before a traumatic event has occurred,” she said. By scanning the adolescents’ brains before the bombing, she and her fellow researchers were able to show that “amygdala reactivity before a traumatic event predicts your response to that traumatic event.”
While two-thirds of Americans will be exposed to some kind of traumatic event during their lifetime, most, fortunately, will not develop PTSD.
“The more we understand the underlying neurobiological systems that shape reactions to traumatic events, the closer we move to understanding a person’s increased vulnerability to them,” McLaughlin said. “That could help us develop early interventions to help people who might develop PTSD later.”
(Source: washington.edu)
L-dopa medication could be helpful in the treatment of phobias and post-traumatic stress disorder
A drug used to treat Parkinson’s disease could also help people with phobias or post-traumatic stress disorder (PTSD). Scientists of the Translational Neurosciences (FTN) Research Center at Johannes Gutenberg University Mainz (JGU) are currently exploring the effects of psychotherapy to extinguish fears in combination with L-dopa. This drug does not only help movement disorders, but might also be used to override negative memories.
Professor Raffael Kalisch, head of the Neuroimaging Center (NIC) of the JGU Translational Neurosciences Research Center, and his collaborators at the University of Innsbruck are conducting research in mice and in humans into the psychological and neurobiological mechanisms of anxiety and fear. “Fear reactions are essential to health and survival, but the memories of angst-inducing situations may cause long-term anxiety or phobias,” explained Kalisch. In psychotherapy, the ’fear extinction’ method is used in exposing people to a threat but without the adverse consequences. Latest research has proven that extinguishing fear also predicts mental health after trauma, suggesting extinction may be an important resilience mechanism.
Fear extinction involves a person being presented with a neutral stimulus, such as a circle on a screen, together with a painful sensation. Soon the person predicts pain in response to the circle on the screen and fear becomes conditioned. Then the person is shown the circle again, but this time without the painful stimulus, so that the person can disassociate the two factors. A person who is afraid of spiders, for example, will in psychotherapy be confronted with spiders in a way that reassures them that the spider is harmless.
In another research program, Belgian scientists tested the ability to extinguish fear in soldiers later deployed to a war zone and found differences in the soldiers’ resilience to traumatic memories. Some experienced post-traumatic stress symptoms following their deployment, whereas those who were able to extinguish fear in the laboratory maintained a good state of mental health. “If you are mentally flexible enough to change the associations that your mind has created, you might be better able to avoid lasting damage,” explained Kalisch. In cooperation with other scientists, Kalisch has found first evidence that this process of changing negative associations might involve the brain’s systems for reward and pleasure and depend on release of the neurotransmitter dopamine that helps control them.
However, even after successful extinction, old fear associations can return under other stressful circumstances. This might involve the development of PTSD or a relapse after successful psychotherapy. Kalisch has found that L-dopa, a drug to treat Parkinson’s disease, can prevent this effect and could therefore possibly be used to prevent relapse in treated PTSD or phobia patients. L-dopa is taken up by the brain and transformed into dopamine that not only controls the brain’s reward and pleasure centers and helps regulate movement, but also affects memory formation. The person receiving L-dopa after extinction will thus create a stronger secondary positive memory of the extinction experience and will thus be able to more easily replace the negative memory. This raises new questions about the role of primary fear memories and secondary prevention by L-dopa. “We would like to be able to enhance the long-term effects of psychotherapy by combining it with L-dopa,” said Professor Raffael Kalisch. To this end, he is about to start a clinical study of people with a spider phobia to determine the effects of L-dopa on therapy outcome. “Manipulating the dopamine system in the brain is a promising avenue to boost primary and secondary preventive strategies based on the extinction procedure,” he continued.
Publication:
Raczka, K. A. et al. (2011), Empirical support for an involvement of the mesostriatal dopamine system in human fear extinction, Translational Psychiatry 1:e12
Haaker, J. et al. (2013), Single dose of L-dopa makes extinction memories context-independent and prevents the return of fear, PNAS Plus - Biological Sciences - Psychological and Cognitive Sciences 110 (26): E2428-36
(Source: uni-mainz.de)
The anatomy of fear: Understanding the biological underpinnings of anxiety, phobias and PTSD
Fear in a mouse brain looks much the same as fear in a human brain.
When a frightening stimulus is encountered, the thalamus shoots a message to the amygdala — the primitive part of the brain — even before it informs the parts responsible for higher cognition. The amygdala then goes into its hard-wired fight-or-flight response, triggering a host of predictable symptoms, including racing heart, heavy breathing, startle response, and sweating.
The similarities of fear response in the brains of mice and men have allowed scientists to understand the neural circuitry and molecular processes of fear and fear behaviors perhaps better than any other response. That understanding has spurred breakthroughs in treatments for psychiatric disorders that are underpinned by fear.
Anxiety disorders are one of the most common mental illnesses in the country, with nearly one-third of Americans experiencing symptoms at least once during their lives. There are generalized anxiety disorders and fear-related disorders, which include panic disorders, phobias, and post-traumatic stress disorder (PTSD).
Emory psychiatrist and researcher Kerry Ressler is on the front lines of fear-disorder research. In his lab at Yerkes National Primate Research Center, he studies the molecular and cellular mechanisms of fear learning and extinction in mouse models. At Grady Memorial Hospital, he investigates the psychology, genetics, and biology of PTSD. And through the Grady Trauma Project, he works to draw attention to the problem of inner city intergenerational violence.
"If you look at Kerry’s work, it can seem like it’s all over the place — he’s got so many studies going on, and he collaborates with so many other scientists," says Barbara Rothbaum, associate vice chair of clinical research in psychiatry and director of the Trauma and Anxiety Recovery Program at Emory. "But they are all pieces to the same puzzle. All his work, from molecular to clinical to policy, fits together and starts telling a story." A Howard Hughes Medical Institute investigator, Ressler was recently elected to the Institute of Medicine — one of the highest honors in the fields of health and medicine. He was named a member of a new national PTSD consortium led by Draper Laboratory. And he recently appeared on the Charlie Rose show’s brain series.
Panic attacks seem to tie the fear-related disorders together, he explained on Charlie Rose. Everyone experiences fear, which evolved as a survival mechanism, but it only rises to a clinical level when people are unable to function normally in the face of it. For instance, PTSD includes not only intrusive thoughts, memories, nightmares, and startle responses, but also the concept of avoidance, which may extend to other areas of the individual’s life.
"There’s a patient I’ve seen who was attacked in a dark alley," Ressler shared on the show. "Initially it just felt dangerous to go out at night, but after a while she grew afraid of men and couldn’t go to that part of town. Then she couldn’t leave her house, and finally, her bedroom. The world got more and more dangerous."
Portable brain-mapping device allows researchers to ‘see’ where memory fails student veterans
UT Arlington researchers have successfully used a portable brain-mapping device to show limited prefrontal cortex activity among student veterans with Post Traumatic Stress Disorder when they were asked to recall information from simple memorization tasks.
The study by bioengineering professor Hanli Liu and Alexa Smith-Osborne, an associate professor of social work, and two other collaborators was published in the May 2014 edition of NeuroImage: Clinical. The team used functional near infrared spectroscopy to map brain activity responses during cognitive activities related to digit learning and memory retrial.
Smith-Osborne has used the findings to guide treatment recommendations for some veterans through her work as principal investigator for UT Arlington’s Student Veteran Project, which offers free services to veterans who are undergraduates or who are considering returning to college.
“When we retest those student veterans after we’ve provided therapy and interventions, they’ve shown marked improvement,” Smith-Osborne said. “The fNIRS data have shown improvement in brain functions and responses after the student veterans have undergone treatment.”
Liu said this type of brain imaging allows us to “see” which brain region or regions fail to memorize or recall learned knowledge in student veterans with PTSD.
“It also shows how PTSD can affect the way we learn and our ability to recall information, so this new way of brain imaging advances our understanding of PTSD.” Liu said.
This study is multi-disciplinary, associating objective brain imaging with neurological disorders and social work.
While UT Arlington bioengineering faculty associate Fenghua Tian is the primary author assisted by bioengineering graduate research assistant Amarnath Yennu, collaborators of the study include UT Austin psychology professor Francisco Gonzalez-Lima and psychology professor Carol North with UT Southwestern Medical Center and the Veterans Administration North Texas Health Care System.
Khosrow Behbehani, dean of the UT Arlington College of Engineering, said this collaborative research is “allowing the researchers to objectively measure the changes in the level of oxygen in the brain and relate them to some of the brain functions that may have been adversely affected by trauma or stress.”
Numerous neuropsychological studies have linked learning dysfunctions – such as memory loss, attention deficits and learning disabilities – with PTSD.
The new study involved 16 combat veterans previously diagnosed with PTSD who were experiencing distress and functional impairment affecting cognitive and related academic performance. The veterans were directed to perform a series of number-ordering tasks on a computer while researchers monitored their brain activity through near infrared spectroscopy, a noninvasive neuroimaging technology.
The research found that participants with PTSD experienced significant difficulty recalling the given digits compared with a control group. This deficiency is closely associated with dysfunction of a portion in the right frontal cortex. The team also determined that near infrared spectroscopy was an effective tool for measuring cognitive dysfunction associated with PTSD.
With that information, Smith-Osborne said mental healthcare providers could customize a treatment plan best suited for that individual.
“It’s not a one-size-fits-all treatment plan but a concentrated effort to tailor the treatment based on where that person is on the learning scale,” Smith-Osborne said.
Smith-Osborne and Liu hope that their research results lead to better and more comprehensive care for veterans and a better college education.
(Source: uta.edu)
Researcher Discovers the Mechanisms That Link Brain Alertness and Increased Heart Rate
George Washington University (GW) researcher David Mendelowitz, Ph.D., was recently published in the Journal of Neuroscience for his research on how heart rate increases in response to alertness in the brain. Specifically, Mendelowitz looked at the interactions between neurons that fire upon increased attention and anxiety and neurons that control heart rate to discover the “why,” “how,” and “where to next” behind this phenomenon.
“This study examines how changes in alertness and focus increase your heart rate,” said Mendelowitz, vice chair and professor of pharmacology and physiology at the GW School of Medicine and Health Sciences. “If you need to focus on a new task at hand, or suddenly need to become more alert, your heart rate increases. We sought to understand the mechanisms of how that happens.”
While the association between vigilance and increased heart rate is long accepted, the neurobiological link had not yet been identified. In this study, Mendelowitz found that locus coeruleus (LC) noradrenergic neurons — neurons critical in generating alertness — directly influence brainstem parasympathetic cardiac vagal neurons (CVNs) — neurons responsible for controlling heart rate. LC noradrenergic neurons were shown to inhibit the brainstem CVNs that generate parasympathetic activity to the heart. The receptors activated within this pathway may be targets for new drug therapies to promote slower heart rates during heightened states.
“Our results have important implications for how we may treat certain conditions in the future, such as post-traumatic stress disorder, chronic anxiety, or even stress,” said Mendelowitz. “Understanding how these events alter the cardiovascular system gives us clues on how we may target these pathways in the future.”
(Source: smhs.gwu.edu)
New study links inflammation in those with PTSD to changes in microRNA
With a new generation of military veterans returning home from Iraq and Afghanistan, post-traumatic stress disorder (PTSD) has become a prominent concern in American medical institutions and the culture at-large. Estimates indicate that as many as 35 percent of personnel deployed to Iraq and Afghanistan suffer from PTSD. New research from the University of South Carolina School of Medicine is shedding light on how PTSD is linked to other diseases in fundamental and surprising ways.
The rise in PTSD has implications beyond the impact of the psychiatric disorder and its immediate consequences, which include elevated suicide risk and inability to lead a normal life, that result in approximately $3 billion in lost productivity every year. Over time, these PTSD patients will continue to experience increased risks of a myriad of medical conditions like cardiovascular disease, diabetes, gastrointestinal disease, fibromyalgia, musculoskeletal disorders and others, all of which share chronic inflammation as a common underlying cause.
The mechanisms that trigger PTSD, and that cause PTSD patients to suffer from higher rates of chronic-inflammation-related medical conditions remain unknown. Additionally, PTSD is incurable, and though there are available treatments, they are often not completely effective. In an effort to get to the root of PTSD, and begin to understand the links between PTSD and the secondary diseases that often come with it, a team at the University of South Carolina School of Medicine is investigating PTSD through the lens of inflammation. They have recently published findings of a new study, “Dysregulation in microRNA Expression is Associated with Alterations in Immune Functions in Combat Veterans with Post-traumatic Stress Disorder,” in the journal PLOS ONE.
In this study, led by Drs. Prakash Nagarkatti and Mitzi Nagarkatti, the authors investigated microRNA profiles and tried to establish a link between the microRNA and inflammation in combat veterans of the Persian Gulf, Iraq and Afghanistan wars who are PTSD patients at the Dorn VA Medical Center. MicroRNA are small, noncoding RNA that can switch human genes on and off, effectively controlling gene expression. Some specific types of microRNA are known to regulate genes involved in inflammation, making them a kind of marker that can indicate when inflammation is present.
The microRNA role in PTSD has not been investigated previous to this study, which found that the PTSD patients had significant alterations in microRNA expression. The study analyzed 1163 microRNA and found that the expression of microRNA that regulate genes involved in inflammation were altered in PTSD patients. The alterations were found to be linked to heightened inflammation in these patients.
Dr. Mitzi Nagarkatti sums up the significance of this study as follows: “We are very excited about these results. Thus far, no one had looked at the role of microRNA in the blood of PTSD patients. Thus, our finding that the alterations in these small molecules are connected to higher inflammation seen in these patients is very interesting and helps establish the connection between war trauma and microRNA changes.”
In addition to the alterations in microRNA expression, the study also found that PTSD patients had higher levels of inflammation caused by certain types of immune cells called T cells. These T cells produced higher levels of inflammatory mediators called cytokines, specifically interferon-gamma and interleukin-17. This finding was especially interesting because one of the inflammation-associated microRNAs, miR-125a, which specifically targets increased production of interferon-gamma, was found to have decreased expression in the PTSD patients studied. Overall, these results suggested that trauma may cause alterations in the expression of microRNA which promote inflammation in PTSD patients.
Commenting on this, Dr. Prakash Nagarkatti said, “These studies form the foundation to further analyze the role of microRNA in PTSD. Trauma experienced during war may trigger changes in microRNA which may in turn cause various clinical disorders seen in PTSD patients. Our long-term goal is to identify whether PTSD patients express a unique signature profile of microRNA which can be used towards early detection, prevention and treatment of PTSD.”
(Source: eurekalert.org)
Researchers report first findings of virtual reality exposure therapy for veterans with PTSD
A randomized controlled clinical trial of Iraq and Afghanistan veterans with post-traumatic stress disorder (PTSD) found that shorter doses of virtual reality exposure therapy (VRE) reduces PTSD diagnoses and symptoms. The study was published in the April 18, 2014 online edition of the American Journal of Psychiatry.
Researchers at Emory University conducted the study with 156 veterans with combat-related PTSD. After an introductory session, each veteran was randomly assigned to receive d-cycloserine (DCS) (53 subjects), alprazolam (50 subjects), or a placebo (53 subjects) before each of five sessions of VRE.
The study found PTSD symptoms significantly improved from pre- to post-treatment with the VRE therapy and the DCS may enhance the VRE results for those veterans who demonstrated better emotional learning in sessions. In addition to self-reported symptoms, researchers used objective measures of cortisol, a stress hormone, and the startle response, and found reductions in reactivity after treatment. Alprazolam, known more commonly as Xanax, impaired recovery from symptoms.
"D-cycloserine, combined with only five sessions of the virtual reality exposure therapy, was associated with significant improvements in objective measures of startle and cortisol and overall PTSD symptoms for those who showed emotional learning in sessions," says lead researcher Barbara Rothbaum, PhD, professor of psychiatry and behavioral sciences at Emory University School of Medicine and director of the Trauma and Anxiety Recovery Program.
The double-blind, placebo-controlled study consisted of an initial screening assessment, six treatment visits, and follow-up assessments at three, six and 12 months post-treatment. The virtual reality exposure therapy involved 30-45 minutes of exposure to virtual environments on a head mounted video display that attempt to match stimuli described by the veteran. Scenes depict a variety of Iraq and Afghanistan environments, including street scenes and neighborhoods, as well as from different points of view, i.e. as a driver, passenger, or walking on foot. Thirty minutes before each session, participants took a single pill.
"We were very excited to see the substantial gains in self-reported and objective indices of PTSD with only five sessions of the virtual reality exposure therapy combined," says Rothbaum.
Computer Maps 21 Distinct Emotional Expressions—Even “Happily Disgusted”
Researchers at The Ohio State University have found a way for computers to recognize 21 distinct facial expressions—even expressions for complex or seemingly contradictory emotions such as “happily disgusted” or “sadly angry.”
(Image caption: Researchers at the Ohio State University have found a way for computers to recognize 21 distinct facial expressions — even expressions for complex or seemingly contradictory emotions. The study gives cognitive scientists more tools to study the origins of emotion in the brain. Here, a study participant makes three faces: happy (left), disgusted (center), and happily disgusted (right). Credit: Image courtesy of The Ohio State University.)
In the current issue of the Proceedings of the National Academy of Sciences, they report that they were able to more than triple the number of documented facial expressions that researchers can now use for cognitive analysis.
“We’ve gone beyond facial expressions for simple emotions like ‘happy’ or ‘sad.’ We found a strong consistency in how people move their facial muscles to express 21 categories of emotions,” said Aleix Martinez, a cognitive scientist and associate professor of electrical and computer engineering at Ohio State. “That is simply stunning. That tells us that these 21 emotions are expressed in the same way by nearly everyone, at least in our culture.”
The resulting computational model will help map emotion in the brain with greater precision than ever before, and perhaps even aid the diagnosis and treatment of mental conditions such as autism and post-traumatic stress disorder (PTSD).
Study in Mice Raises Question: Could PTSD Involve Immune Cell Response to Stress?
Chronic stress that produces inflammation and anxiety in mice appears to prime their immune systems for a prolonged fight, causing the animals to have an excessive reaction to a single acute stressor weeks later, new research suggests.
After the mice recovered from the effects of chronic stress, a single stressful event 24 days later quickly returned them to a chronically stressed state in biological and behavioral terms. Mice that had not experienced the chronic stress were unaffected by the single acute stressor.
The study further showed that immune cells called to action as a result of chronic stress ended up on standby in the animals’ spleens and were launched from that organ to respond to the later stressor.
Mice without spleens did not experience the same reactivation with the second stressor, signifying the spleen’s role as a reservoir for primed immune cells to remain until they’re activated in response to another stressor.
The excessive immune response and anxiety initiated by a brief stressor mimic symptoms of post-traumatic stress disorder.
The Ohio State University scientists are cautious about extending their findings to humans. But they say their decade of work with this model of stress suggests that the immune system has a significant role in affecting behavior. And they are the first to study this re-establishment of anxiety in animals with a later acute stressor.
“No one else has done a study of this length to see what happens to recovered animals if we subject them again to stress,” said Jonathan Godbout, a lead author of the study and associate professor of neuroscience at Ohio State. “That retriggering is a component of post-traumatic stress. The previously stressed mice are living a normal rodent life, and then this acute stress brings everything back. Animals that have never been exposed to stress before were unaffected by that one event – it didn’t change behavioral or physiological properties.”
The research is published online in the journal Biological Psychiatry.
(Source: researchnews.osu.edu)