News Topic PTSD
About these topic collections
I’ve been reporting on memory research for over ten years and these topic pages are simply collections of all the news items I have made on a particular topic. They do not pretend to be in any way exhaustive! I cover far too many areas within memory to come anywhere approaching that. What I aim to do is provide breadth, rather than depth. Outside my own area of cognitive psychology, it is difficult to know how much weight to give to any study (I urge you to read my blog post on what constitutes scientific evidence). That (among other reasons) is why my approach in my news reporting is based predominantly on replication and consistency. It's about the aggregate. So here is the aggregate of those reports I have at one point considered of sufficient interest to discuss. If you know of any research you would like to add to the collection, feel free to write about it in a comment (please provide a reference).
A study involving 520 intensive care patients who had been put on ventilators for acute lung injury (ALI), of whom 186 patients of the 275 survivors were followed up over the next two years, found that 35% of them had clinically significant symptoms of PTSD. Nearly two-thirds of these (62%) still had symptoms at two years.
ICU survivors with PTSD are unusual in that they often experience flashbacks to delusions or hallucinations they had in the hospital, rather than events that actually occurred
The main risk factors were: depression before hospitalization; greater length of time in the ICU; development of sepsis while in ICU; high doses of opiates. Lowered risk was associated with being given corticosteroids.
 Post-traumatic stress disorder symptoms after acute lung injury: a 2-year prospective longitudinal study. Psychological Medicine. FirstView, 1 - 15.(2013).
It certainly sounds like pseudo-science, but that's why we do science - because the weirdness of something is not a particularly good reason to dismiss it (quantum! many-universes!). Sometimes we don't understand enough about how things work to know why they work, but finding out whether or not they work is a good place to start.
Tori Rodriguez at Scientific American:
Imagine you are trying to put a traumatic event behind you. Your therapist asks you to recall the memory in detail while rapidly moving your eyes back and forth, as if you are watching a high-speed Ping-Pong match. The sensation is strange, but many therapists and patients swear by the technique, called eye movement desensitization and reprocessing (EMDR). Although skeptics continue to question EMDR's usefulness, recent research supports the idea that the eye movements indeed help to reduce symptoms of post-traumatic stress disorder (PTSD).
We know that emotion affects memory. We know that attention affects perception (see, e.g., Visual perception heightened by meditation training; How mindset can improve vision). Now a new study ties it all together. The study shows that emotionally arousing experiences affect how well we see them, and this in turn affects how vividly we later recall them.
The study used images of positively and negatively arousing scenes and neutral scenes, which were overlaid with varying amounts of “visual noise” (like the ‘snow’ we used to see on old televisions). College students were asked to rate the amount of noise on each picture, relative to a specific image they used as a standard. There were 25 pictures in each category, and three levels of noise (less than standard, equal to standard, and more than standard).
Different groups explored different parameters: color; gray-scale; less noise (10%, 15%, 20% as compared to 35%, 45%, 55%); single exposure (each picture was only presented once, at one of the noise levels).
Regardless of the actual amount of noise, emotionally arousing pictures were consistently rated as significantly less noisy than neutral pictures, indicating that people were seeing them more clearly. This was true in all conditions.
Eye-tracking analysis ruled out the idea that people directed their attention differently for emotionally arousing images, but did show that more eye fixations were associated both with less noisy images and emotionally arousing ones. In other words, people were viewing emotionally important images as if they were less noisy.
One group of 22 students were given a 45-minute spatial working memory task after seeing the images, and then asked to write down all the details they could remember about the pictures they remembered seeing. The amount of detail they recalled was taken to be an indirect measure of vividness.
A second group of 27 students were called back after a week for a recognition test. They were shown 36 new images mixed in with the original 75 images, and asked to rate them as new, familiar, or recollected. They were also asked to rate the vividness of their recollection.
Although, overall, emotionally arousing pictures were not more likely to be remembered than neutral pictures, both experiments found that pictures originally seen as more vivid (less noise) were remembered more vividly and in more detail.
Brain scans from 31 students revealed that the amygdala was more active when looking at images rated as vivid, and this in turn increased activity in the visual cortex and in the posterior insula (which integrates sensations from the body). This suggests that the increased perceptual vividness is not simply a visual phenomenon, but part of a wider sensory activation.
There was another neural response to perceptual vividness: activity in the dorsolateral prefrontal cortex and the posterior parietal cortex was negatively correlated with vividness. This suggests that emotion is not simply increasing our attentional focus, it is instead changing it by reducing effortful attentional and executive processes in favor of more perceptual ones. This, perhaps, gives emotional memories their different ‘flavor’ compared to more neutral memories.
These findings clearly need more exploration before we know exactly what they mean, but the main finding from the study is that the vividness with which we recall some emotional experiences is rooted in the vividness with which we originally perceived it.
The study highlights how emotion can sharpen our attention, building on previous findings that emotional events are more easily detected when visibility is difficult, or attentional demands are high. It is also not inconsistent with a study I reported on last year, which found some information needs no repetition to be remembered because the amygdala decrees it of importance.
I should add, however, that the perceptual effect is not the whole story — the current study found that, although perceptual vividness is part of the reason for memories that are vividly remembered, emotional importance makes its own, independent, contribution. This contribution may occur after the event.
It’s suggested that individual differences in these reactions to emotionally enhanced vividness may underlie an individual’s vulnerability to post-traumatic stress disorder.
 Psychophysical and Neural Evidence for Emotion-Enhanced Perceptual Vividness. The Journal of Neuroscience. 32(33), 11201 - 11212.(2012).
A new study has found that, when delivered quickly, a modified form of prolonged exposure therapy reduces post-traumatic stress reactions and depression.
The study involved 137 patients being treated in the emergency room of a major trauma center in Atlanta. The patients were chosen from survivors of traumatic events such as rape, car or industrial accidents, and shooting or knife attacks. Participants were randomly assigned to either receive three sessions of therapy beginning in the emergency department (an average of 12 hours after the event), or assessment only. Stress reactions were assessed at 4 and 12 weeks, and depression at baseline and 4 weeks.
Those receiving the therapy reported significantly lower post-traumatic stress at 4 weeks and 12 weeks, and significantly lower depression at 4 weeks. Analysis of subgroups revealed that the therapy was most effective in rape victims. In the cases of transport accidents and physical (non-sexual) assault, the difference between therapy and assessment-only was only barely significant (for transport at 4 weeks) or non-significant. In both subgroups, the effect was decidedly less at 12 weeks than at 4 weeks.
The therapy, carried out by trained therapists, involved participants describing the trauma they had experienced while the therapist recorded the description. The bulk of the hour-long session was taken up with reliving and processing the experience. There were three sessions spaced a week apart. The patients were instructed to listen to their recordings every day, and 85% were compliant. The therapists also explained normal reactions to trauma, helped the patients look at obtrusive thoughts of guilt or responsibility, and taught them a brief breathing or relaxation technique and self care.
While this study doesn’t itself compare the effects of immediate vs delayed therapy, the assumption that delivering the therapy so soon after the trauma is a crucial factor in its success is in line with other research (mainly to do with fear-conditioning in rodent and human laboratory studies). Moreover, while brief cognitive-behavioral therapy has previously been shown to be effective with people diagnosed with acute stress disorder, such therapy is normally begun some 2-4 weeks after trauma, and a study of female assault survivors found that although such therapy did indeed accelerate recovery compared with supportive counseling, after 9 months, PTSD severity was similar in both groups.
Another, severe, limitation of this study is that the therapy involved multiple items. We cannot assume that it was the repeated re-experiencing of the event that is critical.
However, this study is only a pilot study, and its findings are instructive rather than decisive. But at the least it does support the idea that immediate therapy is likely to help victims of trauma recover more quickly.
One final, important, note: It should not, of course, be assumed that simply having the victim describe the events — say to police officers — is in itself therapeutic. Done badly, that experience may itself be traumatic.
Following previous research suggesting that the volume of the hippocampus was reduced in some people with chronic PTSD, a twin study indicated that this may not be simply a sign that stress has shrunk the hippocampus, but that those with a smaller hippocampus are at greater risk of PTSD. Now a new study has found that Gulf War veterans who recovered from PTSD had, on average, larger hippocampi than veterans who still suffer from PTSD. Those who recovered had hippocampi of similar size to control subjects who had never had PTSD.
The study involved 244 Gulf War veterans, of whom 82 had lifetime PTSD, 44 had current PTSD, and 38 had current depression.
Because we don’t know hippocampal size prior to trauma, the findings don’t help us decide whether hippocampal size is a cause or an effect (or perhaps it would be truer to say, don’t help us decide the relative importance of these factors, because it seems most plausible that both are significant).
The really important question, of course, is whether an effective approach to PTSD treatment would be to work on increasing hippocampal volume. Exercise and mental stimulation, for example, are known to increase the creation of new brain cells in the hippocampus. In this case, the main mediator is probably the negative effects of stress (which reduces neurogenesis). There is some evidence that antidepressant treatment might increase hippocampal volume in people with PTSD.
The other conclusion we can derive from these findings is that perhaps we should not simply think of building hippocampal volume / creating new brain cells as a means of building cognitive reserve, thus protecting us from cognitive decline and dementia. We should also think of it as a means of improving our emotional resilience and protecting us from the negative effects of stress and trauma.
 Hippocampal Volume Differences in Gulf War Veterans with Current Versus Lifetime Posttraumatic Stress Disorder Symptoms. Biological Psychiatry. 69(6), 541 - 548.(2011).
 Smaller hippocampal volume predicts pathologic vulnerability to psychological trauma. Nature neuroscience. 5(11), 1242 - 1247. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2819093/(2002).
Given all the research showing the importance of sleep for consolidating memories, it should come as no great surprise that the reverse is also true: depriving yourself of sleep could help you forget experiences you would prefer not to remember.
In the study, 28 student volunteers were shown 14 short video clips, half of which showed safe driving down a city street, and half showed the car being involved in a nasty crash. Half of the volunteers were then deprived of sleep while the other half received a normal night's sleep. The next day, they were shown pictures and asked to indicate whether they had appeared in the clips they had seen. They were also asked to rate the fear evoked by the image, and their physiological responses measured. They were tested again 3 and 10 days later.
While there was no difference between the two groups in picture recognition, the control group rated the images from the crash videos as fearful, and these responses generalized over time to the other images. However, those who were sleep deprived showed such reactions only on the first day.
The finding suggests a possible therapy for PTSD or other anxiety disorders.
 Sleep Deprivation Facilitates Extinction of Implicit Fear Generalization and Physiological Response to Fear. Biological Psychiatry. 68(11), 991 - 998.(2010).
A mouse study has revealed the brain becomes overly stimulated after a traumatic event causes an ongoing, frenzied interaction between two brain proteins long after they should have disengaged. However, the injection of newly developed drugs into the hippocampus within a five hour window calmed this process, and prevented the development of a post-traumatic fear response.
The new research shows the potential for PTSD occurs when a stressful event causes a flood of glutamate, which then interacts with a second protein (Homer1a). This protein continues to stimulate metabotropic glutamate receptor 5 [mGluR5] after the glutamate has dissipated. The new drugs bind mGluR5 and reverse its activity.
 Metabotropic Glutamate Receptor 5/Homer Interactions Underlie Stress Effects on Fear. Biological Psychiatry. 68(11), 1007 - 1015.(2010).
Following a study showing that playing Tetris after traumatic events could reduce memory flashbacks in healthy volunteers, two experiments have found playing Tetris after viewing traumatic images significantly reduced flashbacks while playing Pub Quiz Machine 2008 (a word-based quiz game) increased the frequency of flashbacks. In the experiments, volunteers were shown a film that included traumatic images of injury.
In the first experiment, after waiting for 30 minutes, 20 volunteers played Tetris for 10 minutes, 20 played Pub Quiz for 10 minutes and 20 did nothing. In the second experiment, this wait was extended to four hours, with 25 volunteers in each group.
In both experiments, those who played Tetris had significantly fewer flashbacks that the other two groups, and all groups were equally able to recall specific details of the film. Flashbacks were monitored for a week.
It is thought that with traumatic information, perceptual information is emphasized over conceptual information, meaning we are less likely to remember the experience of being in a high-speed road traffic collision as a coherent story, and more likely to remember it by the flash of headlights and noise of a crash. This perceptual information then pops up repeatedly in the victim's mind in the form of flashbacks to the trauma causing great emotional distress, as little conceptual meaning has been attached to them. If you experience other events that involve similar information, during the time window in which the traumatic memories are being processed, that information will interfere with that processing.
Thus, the spatial tasks of Tetris (which involves moving and rotating shapes) are thought to compete with the images of trauma, while answering general knowledge questions in the Pub Quiz game competes with remembering the contextual meaning of the trauma, so the visual memories are reinforced and the flashbacks are increased.
 Can Playing the Computer Game “Tetris” Reduce the Build-Up of Flashbacks for Trauma? A Proposal from Cognitive Science. PLoS ONE. 4(1), e4153 - e4153.(2009).
A study involving over 180,000 older veterans (average age 68.8 at study start), of whom 29% had PTSD, has revealed that those with PTSD had a significantly greater risk of developing dementia. Over the seven years of the study, 10.6% of the veterans with PTSD developed dementia compared to 6.6% of those without PTSD. When age was used as the time scale, the risk for those with PTSD was more than double. Results were similar when those with a history of head injury, substance abuse, or clinical depression, were excluded.
One possibility for the link is that the stress induced by PTSD contributes to the development of dementia.
 Posttraumatic Stress Disorder and Risk of Dementia Among US Veterans. Arch Gen Psychiatry. 67(6), 608 - 613.(2010).
A study in which nearly 50 participants consumed either alcohol (.4 or .8 g/kg, around 2 or 4 glasses of wine) or a placebo drink, performed a memory task, then were shown a video of serious road traffic accidents, has found that those given the smaller amount of alcohol experienced more flashbacks during the next week than those given the larger amount of alcohol, and those given no alcohol. Although that may seem to suggest drinking a large amount of alcohol might result in less involuntary re-experiencing of the event, excessive alcohol produced an overall reduction in memory which may be even more distressing if they then imagine a 'worse case scenario.' The findings support the view that flashbacks reflect the reactivation of image-based egocentric representations (based on sensory features) in the absence of a corresponding allocentric representing (incorporating the spatiotemporal context). Alcohol appears to impair allocentric (contextual) memory first.
 Acute Effects of Alcohol on Intrusive Memory Development and Viewpoint Dependence in Spatial Memory Support a Dual Representation Model. Biological Psychiatry. In Press, Corrected Proof,(Submitted).
Older news items (pre-2010) brought over from the old website
An imaging study comparing brain activity during a verbal memory task of 16 10- to 17-year-olds who had PTSD symptoms with a control group of 11 young people, has found that while hippocampal activity was similar in both groups when the word list was presented, those with PTSD symptoms made more errors on the recall part of the test and showed less hippocampus activity than control subjects doing the same task. Additionally, those with the worst hippocampus function were also most likely to experience a specific set of PTSD symptoms — "avoidance and numbing", including difficulty remembering the trauma, feeling cut off from others and lack of emotion. The research helps explain why traumatized children behave as they do and could improve treatments.
 Reduced Hippocampal Activity in Youth with Posttraumatic Stress Symptoms: An fMRI Study. J. Pediatr. Psychol.. jsp112 - jsp112.(2009).
PTSD Linked to Nearly Double Dementia Risk in Veterans
Data from 181,093 veterans aged 55 years and older without dementia (53,155 veterans diagnosed with PTSD and 127,938 veterans without PTSD) found that PTSD patients were nearly twice as likely to develop incident dementia compared to veterans without PTSD. Results were similar when we excluded those with a history of traumatic brain injury, substance abuse or depression.
Yaffe, K. et al. 2009. Post-traumatic stress disorder and risk of dementia among U.S. veterans. Presented at the Alzheimer's Association International Conference on Alzheimer's Disease July 11-16 in Vienna.
Cognitive therapy useful in treating post-traumatic stress disorder in early stages
A study of 248 adults with early symptoms of post-traumatic stress disorder (PTSD) following a traumatic event that had occurred no more than four weeks earlier (ie before PTSD can be formally diagnosed) compared 12 weeks’ treatment of either cognitive therapy (which helps people change unproductive or harmful thought patterns), cognitive behavioral therapy (which helps desensitize patients’ upsetting reactions to traumatic memories), an antidepressant (selective serotonin reuptake inhibitor) known to be helpful in treating chronic PTSD, placebo or no intervention at all. It was found that symptoms of PTSD were significantly less severe in those who received cognitive therapy or cognitive behavioral therapy compared to those treated with medication, placebo, or no treatment at all.
The study was presented at the American College of Neuropsychopharmacology (ACNP) annual meeting.
Some brain injuries may reduce the likelihood of PTSD
A study of combat-exposed Vietnam War veterans shows that those who suffered injuries to the amygdala or the ventromedial prefrontal cortex were less likely to develop post-traumatic stress disorder than those who suffered damage in other areas or had no head injuries (in fact none of those whose amygdala was damaged developed PTSD). The findings suggest that treatment designed to inhibit the activity of these two areas might provide relief from PTSD.
 Focal brain damage protects against post-traumatic stress disorder in combat veterans. Nat Neurosci. 11(2), 232 - 237.(2008).
Effectiveness of most PTSD therapies is uncertain
A review of 53 studies of pharmaceuticals and 37 studies of psychotherapies used in PTSD treatment has concluded that because of shortcomings in many of the studies, there is not enough reliable evidence to draw conclusions about the effectiveness of most treatments. However, sufficient evidence exists to conclude that exposure therapies — such as exposing individuals to a real or surrogate threat in a safe environment to help them overcome their fears — are effective.
Work could lead to first drug for post-traumatic stress disorder
Researchers have found the molecular mechanism that governs the formation of fears stemming from traumatic events. It was found that inhibiting a kinase (kinases are enzymes that change proteins) called Cdk5 facilitates the extinction of fear learned in a particular context, while increasing that kinase's activity in the hippocampus led to the fear persisting. The work could lead to the first drug to treat PTSD.
 A hippocampal Cdk5 pathway regulates extinction of contextual fear. Nat Neurosci. 10(8), 1012 - 1019.(2007).
Anticipation strengthens memory
An imaging study has revealed that the amygdala and the hippocampus become activated when a person is anticipating a difficult situation (some type of gruesome picture). Moreover, the higher the level of activation during this anticipation, the better the pictures were remembered two weeks later. The study demonstrates how expectancy can affect long-term memory formation, and suggests that the greater our anxiety about a situation, the better we’ll remember that situation. If it’s an unpleasant one, this will only reinforce the anxiety, setting up a vicious cycle. The study has important implications for the treatment of psychological conditions such as post-traumatic stress disorder and social anxiety.
 The effect of anticipation and the specificity of sex differences for amygdala and hippocampus function in emotional memory. Proceedings of the National Academy of Sciences. 103(38), 14200 - 14205.(2006).
Prevalence of combat-related PTSD
Two large independent studies funded by the US government have assessed the impact of the Vietnam War on the prevalence of PTSD in US veterans. The National Vietnam Veterans Readjustment Study (NVVRS) estimated prevalence to be 15.2% while the Vietnam Experience Study (VES) estimated the prevalence to be 2.2%. A new study explains this discrepancy by reanalyzing both data sets using varying criteria. Prevalence estimates for combat-related PTSD of 2.5% and 2.9% for the VES and the NVVRS, respectively, were found when a narrow and specific set of criteria were used, while prevalence estimates 12.2% and 15.8% for the VES and NVVRS, respectively, were found when broader and more sensitive criteria were used.
 Reconciling disparate prevalence rates of PTSD in large samples of US male Vietnam veterans and their controls. BMC Psychiatry. 6, 19 - 19.(2006).
Why traumatic memories have the power they do
In the first imaging study to look at retrieval of emotional memories after a long period (one year after encoding), researchers found that people did recall emotional images, both pleasant and unpleasant, better than emotionally-neutral images. This recall was associated with higher activity in both the amygdala and the hippocampus. The synchronicity of activity between these two regions suggested that each region triggers the other, creating a self-reinforcing "memory loop" in which an emotional cue might trigger recall of the event, which then loops back to a re-experiencing of the emotion of the event. The findings suggest why people subject to traumatic events may be trapped in a cycle of emotion and recall that aggravates post-traumatic stress disorder, and may also suggest why therapies in which people relive such memories and reshape perspective to make it less traumatic can help people cope with such memories.
 Remembering one year later: Role of the amygdala and the medial temporal lobe memory system in retrieving emotional memories. Proceedings of the National Academy of Sciences of the United States of America. 102(7), 2626 - 2631.(2005).
Visuospatial tasks during trauma may reduce intrusive memories
In three experiments, researchers found that viewers who performed a visuospatial task (tapping out a specified pattern on a hidden keyboard) while watching a 12.5-minute trauma video with five scenes of horrific content suffered fewer intrusive memories in the following week than viewers who performed a verbal task. This may occur because the same types of memory resources may be involved in processing both particular visuospatial tasks and the sensory aspects of traumatic stimuli. On the other hand, verbal distraction – counting down by threes -- was associated with a greater number of subsequent intrusions, suggesting that verbal interference might interfere with processing that helps the viewer make sense of the traumatic images. While more research is needed, this suggests a hopeful new approach to dealing not only with PTSD but also other psychological disorders now thought to involve intrusive imagery, such as worry (generalized anxiety disorder), insomnia, social phobia, agoraphobia, psychosis and others.
Holmes, E.A., Brewin, C.R. & Hennessy, R.G. 2004. Trauma Films, Information Processing, and Intrusive Memory Development. Journal of Experimental Psychology: General, 133 (1)
Losing consciousness helps prevent PTSD
Current thinking holds that traumatic brain injury alone may be sufficient to protect patients from developing posttraumatic stress disorder, but new research suggests this protection extends chiefly to those who lose consciousness (for a significant period) during their ordeal. The study was small and requires replication with a bigger sample.
Glaesser, J., Neuner, F., Lütgehetmann, R., Schmidt, R. & Elbert, T. 2004. Posttraumatic stress disorder in patients with traumatic brain injury. BMC Psychiatry, 4, 5.
The article is available at: http://www.biomedcentral.com/1471-244X/4/5/abstract
Reducing the trauma of traumatic memories
For some, stressful memories can reawaken intense fear, with undesirable consequences. A new study involving mice has found that such stress induces a change in the expression of the acetylcholinesterase gene, which normally produces a vital protein that adheres to neuronal synapses. Following stress, however, the same gene produces large quantities of a protein with modified properties that results in heightened electrical signals in the nerve cells communicating through these synapses. The effect is to create reactions of extreme fright or immobilizing shock. Later encounter with a context which triggers those stressful memories can set off that same neuronal reaction. The researchers have developed an "antisense" agent that acts to neutralize the process whereby the modified protein is produced, thereby preventing the extreme reaction.
 Stress-induced alternative splicing of acetylcholinesterase results in enhanced fear memory and long-term potentiation. Mol Psychiatry. 9(2), 174 - 183.(2003).