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Differences In Recovered Memories Of Childhood Sexual Abuse

ScienceDaily (Feb. 4, 2009)
When a child experiences a traumatic event, such as sexual abuse, it may not be until well into adulthood that they remember the incident. It is not known how adults are able to retrieve long-forgotten memories of abuse and there has been some controversy as to the authenticity of these reports.

The results of a new study in Psychological Science, a journal of the Association for Psychological Science, suggests that there are important differences between people who gradually recover memories of abuse during suggestive therapy sessions and those who recover memories of abuse more spontaneously. Psychologist Elke Geraerts of the University of St. Andrews and her colleagues reveal that these people are either susceptible to recovering false memories or have a tendency to forget earlier recollections of the abuse.

The study volunteers included 120 women who were classified into four groups, based on their responses during a preliminary interview. The groups were: women who spontaneously recovered memories of childhood sexual abuse on their own, women who gradually recovered memories of childhood sexual abuse during suggestive therapy sessions, women who had never forgotten having been sexually abused and women who had never been sexually abused. All of these women participated in a false-memory test.

They studied a list of related words (such as bed, rest, awake and tired). After a few minutes, they were shown a set of words (which included ones they had studied as well as new words) and had to indicate which words were on the original list.

The results showed that the women who recovered their memories of childhood sexual abuse during suggestive therapy were the most prone to false memories. For instance, women from this group were more likely to select sleep (in the example above) as having been on the original list, when in fact, it was not.

The women then participated in another memory test, which measured the participants’ propensity to forget what they had just remembered. The results of this test revealed that the group who spontaneously recovered memories of childhood sexual abuse was the most likely to forget that they had successfully remembered certain words earlier.

The authors note that their findings argue against the generalization that all recovered memories of childhood sexual abuse are based on false recollections and “that such effects appear to be associated with suggestive therapy, not recovery of childhood sexual abuse in general.” They conclude that this research has important implications for clinicians who treat patients reporting recovered memories of childhood sexual abuse.

The authors suggest that these clinicians should consider the context of the recovered memories to most effectively treat their patients.

Adapted from materials provided by Association for Psychological Science.

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Understanding Posttraumatic Stress Disorder: An Expert Interview With Doug Zatzick, MD

Dr. Barclay: How prevalent is PTSD in the United States and worldwide; how is the prevalence changing with time; and what are the demographics?

Dr. Zatzick: According to the National Comorbidity Survey in 1995,[1] which is one of the best studies of PTSD prevalence in the United States to date, 5% to 10% of US civilians have PTSD at some point during their lifetime (approximately 5% of men and 10% of women). In the population of injured trauma survivors, in whom I do most of my research, about 20% have symptoms consistent with PTSD. We have a paper this month in the Annals of Surgery[2] showing that at 12 months after injury, a little over 20% of injured trauma survivors hospitalized at US level I trauma centers had symptoms consistent with PTSD and about 6% had depression. Both disorders were independently associated with significant impairments across all functional outcomes, including physical function (activities, such as climbing stairs and getting around in the community), social function (interacting with family and friends), and returning to work and productive activity.

There have been many studies of worldwide prevalence of PTSD. In a study of one group of returning veterans of the current Central Asian conflicts, incidence of symptoms consistent with a current diagnosis of PTSD was about 11% to 18%.[3]

Worldwide, there have been a lot of studies in conflict areas where the incidence of PTSD is much, much higher.[4] For civilians in conflict-ridden areas, the incidence of PTSD is very high because of the high prevalence of exposure to recurrent traumatic life events.

Dr. Barclay: What are the clinical challenges involved in diagnosing and managing PTSD overall?

Dr. Zatzick: I work at a level I trauma center that is also an inner-city safety-net hospital. Therefore, I often consult on injured patients, low-income ethnically diverse patients, and first-generation Americans who have immigrated to the United States after experiencing major trauma in their countries of origin. So, for example, in the setting of an outpatient visit for PTSD after a motor vehicle accident in which there were no severe injuries or extreme incidents, such as the death of another person. If such patients are medically stable, with no major preexisting medical or psychiatric problems, and was not exposed to multiple recurrent traumatic events before the injury, and has a good support system and reasonable life circumstances, they should do very well with CBT for PTSD, especially if they are motivated for treatment. Examples of types of CBT for PTSD include exposure and cognitive processing therapy. Medications, particularly the selective serotonin reuptake inhibitors (SSRIs), may also be effective in some patients, although there have been some recent questions about their efficacy in PTSD.

The challenges in management of PTSD are more complicated in alternative real-world scenarios, such as an acute trauma center or combat zone. For example, when an accident survivor has undergone surgery, is being managed in the intensive care unit, has opiates on board for pain, and will be undergoing months of rehabilitation, that’s complicated. There are multiple, competing demands on their time that push the patient in directions where they may not be ready to get psychotherapy, and addressing PTSD in this setting is much more difficult.

In a disaster zone, for example, if the patient has been evacuated, is a refugee and can’t get to [a pharmacy] for a prescription, and can’t get to a therapist’s office because even finding a therapist is a major challenge…

Dr. Barclay: How effective are currently available treatments for PTSD?

Dr. Zatzick: For patients with a single episode of trauma, good social support, no severe or recurrent trauma history, and no comorbid history of substance abuse — who are not avoiding treatment and will come to every CBT session — the odds are that they will respond to CBT. However, the response rate may be much lower if there are a lot of complicating factors. There is some evidence that the specific serotonin uptake inhibitor class of antidepressants may also be efficacious treatments for PTSD (SSRIs), yet the evidence base is not as solid as for CBT. (See American Psychiatric Association PTSD guidelines and British NICE PTSD guidelines.)

Dr. Barclay: What are the safety and tolerability issues with currently available treatments for PTSD?

Dr. Zatzick: The SSRIs have side effects, including headache, sexual side effects, and gastrointestinal upset. Disturbed sleep is often an issue with PTSD itself, and the SSRIs may exacerbate that. There have been some studies showing that prazosin may be useful for nightmares/sleep when given with an SSRI and it is not habit-forming, but it may cause orthostatic hypotension.

Even CBT is not totally free from adverse effects because a lot of people don’t like going back in their imagination and re-experiencing the event. Some patients drop out of therapy because it is so anxiety-provoking, but for those who stick it out, it’s really a great treatment.

Dr. Barclay: Are there new drugs for PTSD in the pipeline, and how do you think they will compare with currently available treatments?

Dr. Zatzick: I mentioned prazosin earlier. For early PTSD interventions I would love to see a drug that would relieve pain right away and also target the anxiety symptoms of PTSD. We see a lot of people at the trauma center who are in pain, so if you can say to them, “here is a medicine that will help your pain today, and in 4-6 weeks it may also help your anxiety,” that would be great. It’s hard to sell starting an SSRI that won’t become effective for 4-6 weeks, especially when that patient already has a lot of opiates on board. Adherence is not likely to be that good. There are other drugs, like propranolol, that work rapidly to lower blood pressure, heart rate, and autonomic response but have no effect on pain, which is the patient’s primary complaint. I would like to see better molecules that simultaneously target pain and anxiety that aren’t habit-forming.

Dr. Barclay: Please comment on the clinical implications of your own research in PTSD, and on directions for future research.

Dr. Zatzick: Our research, set in US level I trauma centers nationwide, is looking at PTSD and functional impairment after injury. We’re trying to improve return to work and other measures of function after traumatic injury and PTSD. We’ve shown that PTSD can affect return to work and other functional ability after injury, and we’re trying to intervene and improve people’s PTSD and reduce their alcohol consumption. PTSD and depression together are really bad in terms of patients being able to return to work.

Dr. Barclay: What is the current burden of PTSD related to the Iraq and Afghanistan wars in terms of prevalence, disability, and healthcare costs?

Dr. Zatzick: I’m currently consulting on grants involving studies of veterans. There are complicated issues in veteran populations concerning being redeployed, multiple recurrent trauma, and comorbid alcohol use.

Dr. Barclay: What role does increasing treatment of active-duty combat troops with psychoactive medications play in PTSD during combat and after discharge?

Dr. Zatzick: I’m not a military psychiatrist, but if I were assigned to a combat unit, I’d be concerned about the side effects of psychoactive medications.

Dr. Barclay: Are there identified factors predisposing troops to PTSD, and are these screened for or should they be screened for before sending troops to combat?

Dr. Zatzick: Luckily, studies are now being done of the National Guard and other troops before they go to combat, so we can get a better idea of factors predisposing troops to PTSD. The big risk factor in both the Vietnam and Iraq conflicts has been shown to be physical injury. Screening for previous psychiatric disorders before deployment may be helpful.

Dr. Barclay: What future directions do you believe are important for PTSD research?

Dr. Zatzick: The genetics of PTSD are important to understand. Optimizing delivery of healthcare services, depending on the target population, is important.

A key point to study is intervention reach, meaning the ability to capture patients in a specified particular target population. If you’ve just been in a motor vehicle accident, for example, and you need a month of rehabilitation, it will take a while for you to get to the psychologist’s or psychiatrist’s office for CBT, so medications might be better in the meantime, and may have greater reach to the target population of interest.

We need to understand how to tailor the intervention to the context of the particular situation. What type of intervention can you do in the Red Cross mental health tent or in a war zone? Future research needs to address stepped collaborative care, meaning how to deal with posttraumatic concerns in their context first, such as reuniting with their family after combat, getting their home back after a hurricane, or getting your wound sewn up and getting antibiotics after a traumatic injury. This type of care management helps us build a therapeutic relationship and gets people into PTSD therapy. So step 1 is engagement, and then evidence-based PTSD treatment follows as step 2.


  1. Kessler RC, Sonnega A, Bromet E, et al. Posttraumatic stress disorder in the National Comorbidity Survey. Arch Gen Psychiatry. 1995;52:1048-1060. Abstract
  2. Zatzick D, Jurkovich GJ, Rivara FP, et al. A national US study of posttraumatic stress disorder, depression, and work and functional outcomes after hospitalization for traumatic injury. Ann Surg. 2008;248:429-437. Abstract
  3. Hoge CW, Castro CA, Messer SC, et al. Combat duty in Iraq and Afghanistan, mental health problems, and barriers to care. N Engl J Med. 2004;351:13-22. Abstract
  4. de Jong JT, Komproe IH, Van Ommeren M, et al. Lifetime events and posttraumatic stress disorder in 4 postconflict settings. JAMA. 2001;286:555-562. Abstract

Interviewer Affiliation: Laurie Barclay, MD, is a freelance reviewer and writer for Medscape.

Interviewee Affiliation: Doug Zatzick, MD, Associate Professor, University of Washington, School of Medicine, Seattle, Washington; Director, Attending Consult Services, Harborview Medical Center, Seattle, Washington

Disclosure for Interviewer: Laurie Barclay, MD, has disclosed no relevant financial relationships.

Disclosure for Interviewee: Doug Zatzick, MD, has disclosed no relevant financial relationships.

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Brain Cells Related To Fear Identified, Paving The Way For More Effective Treatment Of Post-Traumatic Stress And Other Anxiety Disorders

ScienceDaily (July 11, 2008)— The National Institute of Mental Health estimates that in any given year, about 40 million adults (18 or older) will suffer from some form of anxiety disorder, including debilitating conditions such as phobias, panic disorders and post-traumatic stress disorder (PTSD).

It is estimated that nearly 15 percent of U.S. soldiers returning from Iraq and Afghanistan develop PTSD, underscoring the urgency to develop better treatment strategies for anxiety disorders.  These disorders can lead to myriad problems that hinder daily life – or ruin it altogether – such as drug abuse, alcoholism, marital problems, unemployment and suicide.

Functional imaging studies in combat veterans have revealed that the amygdala, a cerebral structure of the temporal lobe known to play a key role in fear and anxiety, is hyperactive in PTSD subjects. Potentially paving the way for more effective treatments of anxiety disorders, a recent Nature report by Denis Paré, professor at the Center for Molecular and Behavioral Neuroscience at Rutgers University in Newark, has identified a critical component of the amygdala’s neural network normally involved in the extinction, or elimination, of fear memories. Paré’s laboratory studies the amygdala and how its activity impacts behavior. His research was published online by Nature on July 9, 2008 and is scheduled to appear in the print edition later in July.

Earlier research has revealed that in animals and humans, the amygdala is involved in the expression of innate fear responses, such as the fear of snakes, along with the formation of new fear memories as a result of experience, such as learning to fear the sound of a siren that predicts an air raid.

In the laboratory, the circuits underlying learned fear are typically studied using an experimental paradigm called Pavlovian fear conditioning. In this research model on rats, a neutral  stimulus such as the sound of a tone elicited a fear response in the rats after they heard it paired with an noxious or unpleasant stimulus, such as a shock to the feet. However, this conditioned fear response was diminished with repetition of the neutral stimulus in the absence of the noxious stimulus. This phenomenon is known as extinction. This approach is similar to that used to treat human phobias, where the subject is presented with the feared object in the absence of danger.

Behavioral studies have demonstrated, however, that extinction training does not completely abolish the initial fear memory, but rather leads to the formation of a new memory that inhibits conditioned fear responses at the level of the amygdala. As such, fear responses can be expressed again when the conditioned stimulus is presented in a context other than the one where extinction training took place.

For example, suppose a rat is trained for extinction in a grey box smelling of roses, and later hears the tone again in a different box, with a different smell and appearance.  The rat will show no evidence of having been trained for extinction. The tone will evoke as much fear as if the rat had not been trained for extinction.

“Extinction memory will only be expressed if tested in the same environment where the extinction training occurred, implying that extinction does not erase the initial fear memory but only suppresses it in a context-specific manner,” notes Paré.

Importantly, it has been found that people with anxiety disorders exhibit an “extinction deficit,” or a failure to “forget.” However, until recently, the mechanisms of extinction have remained unknown.

As reported by Nature, Paré has found that clusters of amygdala cells, known as the intercalated (ITC) neurons, play a key role in extinction. His findings indicate that ITC cells inhibit amygdala outputs to the brain stem structures that generate fear responses. Indeed, Paré and his collaborators have shown that when ITC cells are destroyed with a targeted toxin in rats, extinction memory is impeded, mimicking the behavior seen in PTSD.

 The significance of this finding derives from earlier results suggesting that PTSD reflects an extinction deficit and that the amygdala is hyperactive in this disorder. As a result, it might be possible to compensate for this abnormality and facilitate extinction with pharmacological interventions that enhance the excitability of ITC cells to inhibit amygdala outputs.

Paré’s research is supported by a $1,487,897 grant from the National Institute of Mental Health. The research project was carried out in collaboration with Rutgers graduate students Ekaterina Likhtik and John Apergis-Scoute, post-doctoral student Daniela Popa, and research assistant G. Anthony Fidacaro.

Adapted from materials provided by Rutgers University.

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Psychotherapy Useful In Treating Post-traumatic Stress Disorder In Early Stages

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ScienceDaily (Dec. 9, 2007) — When treated within a month, survivors of a psychologically traumatic event improved significantly with psychotherapy, according to a new study presented at the American College of Neuropsychopharmacology (ACNP) annual meeting. Lead researcher and ACNP member Arieh Shalev, M.D., Chair of the Department of Psychiatry and founding Director of the Center for Traumatic Stress at Hadassah University Hospital in Jerusalem, studied 248 adults with early symptoms of post-traumatic stress disorder (PTSD) following a traumatic event that had occurred no more than four weeks earlier. His goal was to determine which forms of treatment given soon after the traumatic event can prevent the development of chronic PTSD. Officially, PTSD cannot be diagnosed until four weeks after a traumatic event. However, symptoms that occur before four weeks often persist, and effective early intervention may prevent subsequent trauma-related suffering.Patients were treated for 12 weeks with cognitive therapy (which helps people change unproductive or harmful thought patterns), cognitive behavioral therapy (which helps densensitize 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. “We found that cognitive therapy and cognitive behavioral therapy worked well on these patients, whose symptoms and duration of PTSD were compared at the end of 3 months of intervention. At that time, their symptoms were significantly less severe than in patients who were treated with medication, placebo, or no treatment at all,” Shalev says. Shalev added that although antidepressants did not work during this early post-trauma period, it is important to continue exploration of pharmacological interventions for early treatment of PTSD. Shalev says that other research suggests that both pharmacotherapy and cognitive behavioral therapy can be partially effective for PTSD when given three months or more after a traumatic event. He adds that it is important for PTSD survivors to know recovery is still possible even if treatment is not received immediately. Nevertheless, Shalev adds that his results indicate that it is best for survivors to be treated as early as possible. Adapted from materials provided by American College of Neuropsychopharmacology.Need to cite this story in your essay, paper, or report? Use one of the following formats: (X) APA

( ) MLA American College of Neuropsychopharmacology (2007, December 9). Psychotherapy Useful In Treating Post-traumatic Stress Disorder In Early Stages. ScienceDaily. Retrieved December 10, 2007, from­ /releases/2007/12/071208092445.htm

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‘Speed Of Thought’ Guides Brain’s Memory Consolidation

This could be important in understanding the processing of traumatic mmemories

ScienceDaily (Nov. 16, 2007) — Scientists at The University of Arizona have added another piece of the puzzle of how the brain processes memory.

Bruce McNaughton, a professor of psychology and physiology, and his colleague David Euston have shown that, during sleep, the reactivated memories of real-time experiences are processed within the brain at a higher rate of speed. That rate can be as much as six or seven times faster, and what McNaughton calls “thought speed.”

Memory stores patterns of activity in modular form in the brain’s cortex. Different modules in the cortex process different kinds of information – sounds, sights, tastes, smells, etc. The cortex sends these networks of activity to a region called the hippocampus. The hippocampus then creates and assigns a tag, a kind of temporary bar code, that is unique to every memory and sends that signal back to the cortex.

Each module in the cortex uses the tag to retrieve its own part of the activity. A memory of having lunch, for example, would involve a number of modules, each of which might record where the diner sat, what was served, the noise level in the restaurant or the financial transaction to pay for the meal.

But while an actual dining experience might have taken up an hour of actual time, replaying the memory of it would only take 8 to 10 minutes. The reason, McNaughton said, is that the speed of the consolidation process isn’t constrained by the real world physical laws that regulate activity in time and space.

The brain uses this biological trick because there is no way for all of its neurons to connect with and interact with every other neuron. It is still an expensive task for the hippocampus to make all of those connections. The retrieval tags the hippocampus generates are only temporary until the cortex can carry a given memory on its own.

“It’s a slow process,” said McNaughton.

“The initial creation of the tag is made through existing connections. In order to do the rewiring necessary to have the intermodular connections carry the burden takes time. What you have to do is reinstate those memories multiple times. Every time you reinstate the memory, the modules make a little shift in the connection . . . something grows this way, grows that way, a connection gets made here, gets broken there. And eventually, after you do this multiple times, then an optimal set of connections gets constructed,” Mc Naughton said.

The brain is generally thought to do all of this during sleep, specifically slow-wave sleep, when the brain is not busy with processing real-time inputs. McNaughton has developed the technology to record from multiple probes, each of which can track the activity of a dozen or more brain cells.

“We need groups of cells because in order to identify a pattern, you have to look at the collected activity of many neurons,” McNaughton said. His previous research has show that cells that fired during activity prior to sleep, also fired in the same sequential patterns during sleep. During sleep, the hippocampus sends little, 100-millisecond bursts of activity to the cortex as much as three times per second.

What remains is finding an experiment that will enable researchers to demonstrate that changes in the memory reactivation process would affect memory consolidation but not damage the brain in the process.

“The more practical point, I think, is that this methodology, the ability to measure how fast the brain is processing at the level of changing the state of the brain from one 10- millisecond epoch to the next, how fast the internal state is sweeping through its memories or its allowable patterns is, I think, a model for thought speed,” McNaughton said.

Knowing the determinants for the speed of thought, he said, might allow studies of the effects of drugs, developmental anomalies and the behavioral therapies that might improve them.

Adapted from materials provided by University of Arizona.

 University of Arizona (2007, November 16). ‘Speed Of Thought’ Guides Brain’s Memory Consolidation. ScienceDaily. Retrieved November 17, 2007, from­ /releases/2007/11/071115164450.htm

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