Older news items (pre-2010) brought over from the old website
Children’s PTSD symptoms linked to poor hippocampus function
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.
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.
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.
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.
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.
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.
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.