Posts tagged PTSD
Articles and news from the latest research reports.
Modifying the activity of neuronal networks that encode spatial memories leads to the formation of an incorrect fear memory in mice
The formation and retrieval of memories allows all kinds of organisms, including humans, to learn and thrive in their environment. Yet our memories are not always accurate, and mistaken remembrances can have important consequences, such as in the justice system and in our navigation of the world. Susumu Tonegawa, Steve Ramirez, Xu Liu and colleagues at the RIKEN-MIT Center for Neural Circuit Genetics, have gained insight into the creation of mistaken memories by using light activation of neurons to generate an incorrect fear memory in mice.
The researchers allowed mice to explore a novel location and used genetic techniques to label neurons in the hippocampus—a part of the brain linked to spatial memory—that were activated in the process with a special channel called channelrhodopsin-2. The cells that expressed this channel could then be artificially activated by light. In this way, the researchers were able to reactivate neurons that fired in that particular location, even if the mice were no longer there.
They then moved the mice to another location where they were exposed to foot shocks, causing the mice to exhibit immobility, a fear behavior. At the same time, the researchers used light to activate the channelrhodopsin-2-expressing neurons that had fired in the first location.
When Tonegawa and his colleagues moved the animals to a third location, they did not show fear behavior. Yet when the mice went back to the first location, where they had never experienced a foot shock, the mice now exhibited prominent freezing behavior. The researchers had generated a ‘false memory’ in the mice of foot shocks in a location in which they had never been exposed to them.
The researchers showed that light reactivation of neuronal networks in the central area of the hippocampus, called the dentate gyrus, could create false memories, while reactivation of the outer ‘CA1’ area of the hippocampus could not. Tonegawa and his colleagues suggest that this is because mouse exploration of different locations leads to activation of more overlapping neuronal networks in the CA1 than in the dentate gyrus. “This may reflect the fundamental differences of how memories are encoded in these two regions,” explains Liu.
The findings provide insight into how the brain encodes and processes memories and could one day lead to treatments for post-traumatic stress disorder. “Our work may also have implications for situations where patients mix reality with their own imaginations, such as in schizophrenia,” says Liu.
Study Suggests Possibility of Selectively Erasing Unwanted Memories
The human brain is exquisitely adept at linking seemingly random details into a cohesive memory that can trigger myriad associations—some good, some not so good. For recovering addicts and individuals suffering from post-traumatic stress disorder (PTSD), unwanted memories can be devastating. Former meth addicts, for instance, report intense drug cravings triggered by associations with cigarettes, money, even gum (used to relieve dry mouth), pushing them back into the addiction they so desperately want to leave.
Now, for the first time, scientists from the Florida campus of The Scripps Research Institute (TSRI) have been able to erase dangerous drug-associated memories in mice and rats without affecting other more benign memories.
The surprising discovery, published this week online ahead of print by the journal Biological Psychiatry, points to a clear and workable method to disrupt unwanted memories while leaving the rest intact.
“Our memories make us who we are, but some of these memories can make life very difficult,” said Courtney Miller, a TSRI assistant professor who led the research. “Not unlike in the movie Eternal Sunshine of the Spotless Mind, we’re looking for strategies to selectively eliminate evidence of past experiences related to drug abuse or a traumatic event. Our study shows we can do just that in mice — wipe out deeply engrained drug-related memories without harming other memories.”
Changing the Structure of Memory
To produce a memory, a lot has to happen, including the alteration of the structure of nerve cells via changes in the dendritic spines—small bulb-like structures that receive electrochemical signals from other neurons. Normally, these structural changes occur via actin, the protein that makes up the infrastructure of all cells.
In the new study, the scientists inhibited actin polymerization—the creation of large chainlike molecules—by blocking a molecular motor called myosin II in the brains of mice and rats during the maintenance phase of methamphetamine-related memory formation.
Behavioral tests showed the animals immediately and persistently lost memories associated with methamphetamine—with no other memories affected.
In the tests, animals were trained to associate the rewarding effects of methamphetamine with a rich context of visual, tactile and scent cues. When injected with the inhibitor many days later in their home environment, they later showed a complete lack of interest when they encountered drug-associated cues. At the same time, the response to other memories, such as food rewards, was unaffected.
While the scientists are not yet sure why powerful methamphetamine-related memories are also so fragile, they think the provocative findings could be related to the role of dopamine, a neurotransmitter involved in reward and pleasure centers in the brain and known to modify dendritic spines. Previous studies had shown dopamine is released during both learning and drug withdrawal. Miller adds, “We are focused on understanding what makes these memories different. The hope is that our strategies may be applicable to other harmful memories, such as those that perpetuate smoking or PTSD.”
(Source: scripps.edu)
Brain circuit can tune anxiety
New findings may help neuroscientists pinpoint better targets for antianxiety treatments.
Anxiety disorders, which include posttraumatic stress disorder, social phobias and obsessive-compulsive disorder, affect 40 million American adults in a given year. Currently available treatments, such as antianxiety drugs, are not always effective and have unwanted side effects.
To develop better treatments, a more specific understanding of the brain circuits that produce anxiety is necessary, says Kay Tye, an assistant professor of brain and cognitive sciences and member of MIT’s Picower Institute for Learning and Memory.
“The targets that current antianxiety drugs are acting on are very nonspecific. We don’t actually know what the targets are for modulating anxiety-related behavior,” Tye says.
In a step toward uncovering better targets, Tye and her colleagues have discovered a communication pathway between two brain structures — the amygdala and the ventral hippocampus — that appears to control anxiety levels. By turning the volume of this communication up and down in mice, the researchers were able to boost and reduce anxiety levels.
Lead authors of the paper, which appears in the Aug. 21 issue of Neuron, are technical assistant Ada Felix-Ortiz and postdoc Anna Beyeler. Other authors are former research assistant Changwoo Seo, summer student Christopher Leppla and research scientist Craig Wildes.
Measuring anxiety
Both the hippocampus, which is necessary for memory formation, and the amygdala, which is involved in memory and emotion processing, have previously been implicated in anxiety. However, it was unknown how the two interact.
To study those interactions, the researchers turned to optogenetics, which allows them to engineer neurons to turn their electrical activity on or off in response to light. For this study, the researchers modified a set of neurons in the basolateral amygdala (BLA); these neurons send long projections to cells of the ventral hippocampus.
The researchers tested the mice’s anxiety levels by measuring how much time they were willing to spend in a situation that normally makes them anxious. Mice are naturally anxious in open spaces where they are easy targets for predators, so when placed in such an area, they tend to stay near the edges.
When the researchers activated the connection between cells in the amygdala and the hippocampus, the mice spent more time at the edges of an enclosure, suggesting they felt anxious. When the researchers shut off this pathway, the mice became more adventurous and willing to explore open spaces. However, when these mice had this pathway turned back on, they scampered back to the security of the edges.
Complex interactions
In a study published in 2011, Tye found that activating a different subset of neurons in the amygdala had the opposite effect on anxiety as the neurons studied in the new paper, suggesting that anxiety can be modulated by many different converging inputs.
“Neurons that look virtually indistinguishable from each other in a single region can project to different regions and these different projections can have totally opposite effects on anxiety,” Tye says. “Anxiety is such an important trait for survival, so it makes sense that you want some redundancy in the system. You want a couple of different avenues to modulate anxiety.”
The Neuron study contributes significantly to scientists’ understanding of the roles of the amygdala and hippocampus in anxiety and offers directions for seeking new drug targets, says Joshua Gordon, an associate professor of psychiatry at Columbia University.
“The study specifies a particular connection in the brain as being important for anxiety. One could imagine, then, identifying components of the machinery of that connection — synaptic proteins or ion channels, for example — that are particularly important for amygdala-hippocampal connectivity. If such specific components could be identified, they would be potential targets for novel antianxiety drugs,” says Gordon, who was not part of the research team.
In future studies, the MIT team plans to investigate the effects of the amygdala on other targets in the hippocampus and the prefrontal cortex, which has also been implicated in anxiety. Deciphering these circuits could be an important step toward finding better drugs to help treat anxiety.
Worms May Shed Light on Human Ability to Handle Chronic Stress
New research at Rutgers University may help shed light on how and why nervous system changes occur and what causes some people to suffer from life-threatening anxiety disorders while others are better able to cope.
Maureen Barr, a professor in the Department of Genetics, and a team of researchers, found that the architectural structure of the six sensory brain cells in the roundworm, responsible for receiving information, undergo major changes and become much more elaborate when the worm is put into a high stress environment.
Scientists have known for some time that changes in the tree-like dendrite structures that connect neurons in the human brain and enable our thought processes to work properly can occur under extreme stress, alter brain cell development and result in anxiety disorders like depression and Post Traumatic Stress Disorder affecting millions of Americans each year.
What scientists don’t understand for sure, Barr says, is the cause behind these molecular changes in the brain.
“This type of research provides us necessary clues that ultimately could lead to the development of drugs to help those suffering with severe anxiety disorders,” Barr says.
In the study published today in Current Biology, scientists at Rutgers have identified six sensory nerve cells in the tiny, transparent roundworm, known as the C. elegans and an enzyme called KPC-1/furin which triggers a chemical reaction in humans that is needed for essential life functions like blood-clotting.
While the enzyme also appears to play a role in the growth of tumors and the activation of several types of virus and diseases in humans, in the roundworm the enzyme enables its simple neurons to morph into new elaborately branched shapes when placed under adverse conditions.
Normally, this one-millimeter long worm develops from an embryo through four larval stages before molting into a reproductive adult. Put it under stressful conditions of overcrowding, starvation and high temperature and the worm transforms into an alternative larval stage known as the dauer that becomes so stress-resistant it can survive almost anything – including the Space Shuttle Columbia disaster in 2003 of which they were the only living things to survive.
“These worms that normally have a short life cycle turn into super worms when they go into the dauer stage and can live for months, although they are no longer able to reproduce,” Barr says.
What is so interesting to Barr is that when a perceived threat is over, these tiny creatures and their IL2 neurons transform back to a normal lifespan and reproductive state like nothing had ever happened. Under a microscope, the complicated looking tree-like connectors that receive information are pruned back and the worm appears as it did before the trauma occurred.
This type of neural reaction differs in humans who can suffer from extreme anxiety months or even years after the traumatic event even though they are no longer in a threatening situation.
The ultimate goal, Barr says, is to determine how and why the nervous system responds to stress. By identifying molecular pathways that regulate neuronal remodeling, scientists may apply this knowledge to develop future therapeutics.
(Source: news.rutgers.edu)
Low doses of psychedelic drug erases conditioned fear in mice
Low doses of a psychedelic drug erased the conditioned fear response in mice, suggesting that the agent may be a treatment for post-traumatic stress disorder and related conditions, a new study by University of South Florida researchers found.
The unexpected finding was made by a USF team studying the effects of the compound psilocybin on the birth of new neurons in the brain and on learning and short-term memory formation. Their study appeared online June 2 in the journal Experimental Brain Research, in advance of print publication.
Psilocybin belongs to a class of compounds that stimulate select serotonin receptors in the brain. It occurs naturally in certain mushrooms that have been used for thousands of years by non-Western cultures in their religious ceremonies.
While past studies indicate psilocybin may alter perception and thinking and elevate mood, the psychoactive substance rarely causes hallucinations in the sense of seeing or hearing things that are not there, particularly in lower to moderate doses.
There has been recent renewed interest in medicine to explore the potential clinical benefit of psilocybin, MDMA and some other psychedelic drugs through carefully monitored, evidence-based research.
“Researchers want to find out if, at lower doses, these drugs could be safe and effective additions to psychotherapy for treatment-resistant psychiatric disorders or adjunct treatments for certain neurological conditions,” said Juan Sanchez-Ramos, MD, PhD, professor of neurology and Helen Ellis Endowed Chair for Parkinson’s Disease Research at the USF Health Morsani College of Medicine.
Dr. Sanchez-Ramos and his colleagues wondered about psilocybin’s role in the formation of short-term memories, since the agent binds to a serotonin receptor in the hippocampus, a region of the brain that gives rise to new neurons. Lead author for this study was neuroscientist Briony Catlow, a former PhD student in Dr. Sanchez-Ramos’ USF laboratory who has since joined the Lieber Institute for Brain Development, a translational neuroscience research center located in the Johns Hopkins Bioscience Park.
The USF researchers investigated how psilocybin affected the formation of memories in mice using a classical conditioning experiment. They expected that psilocybin might help the mice learn more quickly to associate a neutral stimulus with an unpleasant environmental cue.
To test the hypothesis, they played an auditory tone, followed by a silent pause before delivering a brief shock similar to static electricity. The mice eventually learned to link the tone with the shock and would freeze, a fear response, whenever they heard the sound.
Later in the study, the researchers played the sound without shocking the mice after each silent pause. They assessed how many times it took for the mice to resume their normal movements, without freezing in anticipation of the shock.
Regardless of the doses administered, neither psilocybin nor ketanserin, a serotonin inhibitor, made a difference in how quickly the mice learned the conditioned fear response. However, mice receiving low doses of psilocybin lost their fearful response to the sound associated with the unpleasant shock significantly more quickly than mice getting either ketanserin or saline (control group). In addition, only low doses of psilocybin tended to increase the growth of neurons in the hippocampus.
“Psilocybin enhanced forgetting of the unpleasant memory associated with the tone,” Dr. Sanchez-Ramos said. “The mice more quickly dissociated the shock from the stimulus that triggered the fear response and resumed their normal behavior.”
The result suggests that psilocybin or similar compounds may be useful in treating post-traumatic stress disorder or related conditions in which environmental cues trigger debilitating behavior like anxiety or addiction, Dr. Sanchez-Ramos said.
1 in 4 Stroke Patients Suffer PTSD
One in four people who survive a stroke or transient ischemic attack (TIA) suffer from symptoms of post-traumatic stress disorder (PTSD) within the first year post-event, and one in nine experience chronic PTSD more than a year later. The data suggest that each year nearly 300,000 stroke/TIA survivors will develop PTSD symptoms as a result of their health scare. The study, led by Columbia University Medical Center researchers, was published today in the online edition of PLOS ONE.
“This work builds on recent findings of ours that PTSD is common among heart attack survivors and that it contributes to a doubled risk of a future cardiac event or of dying within one to three years. Our current results show that PTSD in stroke and TIA survivors may increase their risk for recurrent stroke and other cardiovascular events,” said first author Donald Edmondson, PhD, MPH, assistant professor of behavioral medicine (Center for Behavioral Cardiovascular Health) at CUMC. “Given that each event is life-threatening and that strokes/TIAs add hundreds of millions of dollars to annual health expenditures, these findings are important to both the long-term survival and health costs of these patient populations.”
“PTSD is not just a disorder of combat veterans and sexual assault survivors, but strongly affects survivors of stroke and other potentially traumatic acute cardiovascular events as well,” said Ian M. Kronish, MD, MPH, assistant professor of medicine (Center for Behavioral Cardiovascular Health) and the study’s senior author. “Surviving a life-threatening health scare can have a debilitating psychological impact, and health care providers should make it a priority to screen for symptoms of depression, anxiety, and PTSD among these patient populations.”
Stroke is the fourth-leading cause of death and the top cause of disability in the United States. According to data from the American Stroke Association, nearly 795,000 Americans each year suffer a new or recurrent stroke, and up to an additional 500,000 suffer a TIA.
PTSD is an anxiety disorder initiated by exposure to a traumatic event. Common symptoms include nightmares, avoidance of reminders of the event, and elevated heart rate and blood pressure. Chronic PTSD is a duration of these symptoms for three months or longer (as defined by the DSM-IV).
Since only a few studies have assessed PTSD due to stroke, Drs. Edmondson and Kronish and their colleagues performed the first meta-analysis of clinical studies of stroke- or TIA-induced PTSD. The nine studies in the meta-analysis included a total of 1,138 stroke or TIA survivors.
The study found that 23 percent, or roughly one in four, of the patients developed PTSD symptoms within the first year after their stroke or TIA, with 11 percent, or roughly one in nine, experiencing chronic PTSD more than a year later.
“PTSD and other psychological disorders in stroke and TIA patients appear to be an under-recognized and undertreated problem,” said Dr. Kronish.
“Fortunately, there are good treatments for PTSD,” said Dr. Edmondson. “But first, physicians and patients have to be aware that this is a problem. Family members can also help. We know that social support is a good protective factor against PTSD due to any type of traumatic event.”
“The next step is further research to assess whether mental health treatment can reduce stroke- and TIA-induced PTSD symptoms and help these patients regain a feeling of normalcy and calm as soon as possible after their health scare,” said Dr. Edmondson.
(Source: newsroom.cumc.columbia.edu)
Posttraumatic Stress Disorder Treatment: Genetic Predictor of Response to Exposure Therapy
There is growing evidence that a gene variant that reduces the plasticity of the nervous system also modulates responses to treatments for mood and anxiety disorders. In this case, patients with posttraumatic stress disorder, or PTSD, with a less functional variant of the gene coding for brain-derived neurotrophic factor (BDNF), responded less well to exposure therapy.
This gene has been implicated previously in treatment response. Basic science studies have convincingly shown that BDNF levels are an important modifier of the therapeutic effects of antidepressants in animal models. Other researchers have made similar findings in a small group of depressed patients treated with the rapid-acting antidepressant ketamine. Low BDNF plasma levels also have been linked to poorer effects of cognitive rehabilitation in schizophrenia. BDNF infused directly into the infralimbic prefrontal cortex in rats was found to extinguish conditioned fear, and BDNF levels were found to modulate the amount of fear extinction.
"Findings are accumulating to suggest that BDNF is an important modifier of the responses to a number of clinical interventions, presumably because BDNF is such an important regulator of neuroplasticity, i.e., the ability of the brain to adapt," said Dr. John Krystal, Editor of Biological Psychiatry.
In this study, researchers from Australia and Puerto Rico teamed up to investigate the influence of the BDNF Val66Met genotype on response to exposure therapy in patients with PTSD. They recruited 55 patients, all of whom participated in an 8-week exposure-based cognitive behavior therapy program.
Exposure therapy is currently the most effective treatment for PTSD, although it does not work for everyone. This type of therapy is delivered over multiple one-on-one sessions with a trained therapist, with a goal of reducing patients’ fear and anxiety.
They found that patients with the Met-66 allele of BDNF, compared with patients with the Val/Val allele, showed poorer response to exposure therapy.
"This paper reflects an important and significant advance, in translating recent ground-breaking findings in animal and human neuroscience into clinically anxious populations," said first author Dr. Kim Felmingham.
She added, “Findings from this study support a widely held, but largely untested, hypothesis that extinction is necessary for exposure therapy. It also provides evidence that genotypes influence response to cognitive behavior therapy.”
This finding supports prior evidence and highlights the importance of considering genotypes as potential predictor variables in clinical trials of exposure therapy.
(Source: alphagalileo.org)
Low Doses of THC Can Halt Brain Damage
Extremely low doses of marijuana’s psychoactive component protect brain before and after injury, says TAU researcher
Though marijuana is a well-known recreational drug, extensive scientific research has been conducted on the therapeutic properties of marijuana in the last decade. Medical cannabis is often used by sufferers of chronic ailments, including cancer and post-traumatic stress disorder, to combat pain, insomnia, lack of appetite, and other symptoms.
Now Prof. Yosef Sarne of Tel Aviv University’s Adelson Center for the Biology of Addictive Diseases at the Sackler Faculty of Medicine says that the drug has neuroprotective qualities as well. He has found that extremely low doses of THC — the psychoactive component of marijuana — protects the brain from long-term cognitive damage in the wake of injury from hypoxia (lack of oxygen), seizures, or toxic drugs. Brain damage can have consequences ranging from mild cognitive deficits to severe neurological damage.
Previous studies focused on injecting high doses of THC within a very short time frame — approximately 30 minutes — before or after injury. Prof. Sarne’s current research, published in the journals Behavioural Brain Research and Experimental Brain Research, demonstrates that even extremely low doses of THC — around 1,000 to 10,000 times less than that in a conventional marijuana cigarette — administered over a wide window of 1 to 7 days before or 1 to 3 days after injury can jumpstart biochemical processes which protect brain cells and preserve cognitive function over time.
This treatment, especially in light of the long time frame for administration and the low dosage, could be applicable to many cases of brain injury and be safer over time, Prof. Sarne says.
Conditioning the brain
While performing experiments on the biology of cannabis, Prof. Sarne and his fellow researchers discovered that low doses of the drug had a big impact on cell signalling, preventing cell death and promoting growth factors. This finding led to a series of experiments designed to test the neuroprotective ability of THC in response to various brain injuries.
In the lab, the researchers injected mice with a single low dose of THC either before or after exposing them to brain trauma. A control group of mice sustained brain injury but did not receive the THC treatment. When the mice were examined 3 to 7 weeks after initial injury, recipients of the THC treatment performed better in behavioral tests measuring learning and memory. Additionally, biochemical studies showed heightened amounts of neuroprotective chemicals in the treatment group compared to the control group.
The use of THC can prevent long-term cognitive damage that results from brain injury, the researchers conclude. One explanation for this effect is pre- and post-conditioning, whereby the drug causes minute damage to the brain to build resistance and trigger protective measures in the face of much more severe injury, explains Prof. Sarne. The low dosage of THC is crucial to initiating this process without causing too much initial damage.
Preventative and long-term use
According to Prof. Sarne, there are several practical benefits to this treatment plan. Due to the long therapeutic time window, this treatment can be used not only to treat injury after the fact, but also to prevent injury that might occur in the future. For example, cardiopulmonary heart-lung machines used in open heart surgery carry the risk of interrupting the blood supply to the brain, and the drug can be delivered beforehand as a preventive measure. In addition, the low dosage makes it safe for regular use in patients at constant risk of brain injury, such as epileptics or people at a high risk of heart attack.
Prof. Sarne is now working in collaboration with Prof. Edith Hochhauser of the Rabin Medical Center to test the ability of low doses of THC to prevent damage to the heart. Preliminary results indicate that they will find the same protective phenomenon in relation to cardiac ischemia, in which the heart muscle receives insufficient blood flow.
(Source: aftau.org)
Chronic trauma can inflict lasting damage to brain regions associated with fear and anxiety. Previous imaging studies of people with post-traumatic stress disorder, or PTSD, have shown that these brain regions can over-or under-react in response to stressful tasks, such as recalling a traumatic event or reacting to a photo of a threatening face. Now, researchers at NYU School of Medicine have explored for the first time what happens in the brains of combat veterans with PTSD in the absence of external triggers.
Their results, published in Neuroscience Letters, and presented today at the annual meeting of the American Psychiatry Association in San Francisco, show that the effects of trauma persist in certain brain regions even when combat veterans are not engaged in cognitive or emotional tasks, and face no immediate external threats. The findings shed light on which areas of the brain provoke traumatic symptoms and represent a critical step toward better diagnostics and treatments for PTSD.
A chronic condition that develops after trauma, PTSD can plague victims with disturbing memories, flashbacks, nightmares and emotional instability. Among the 1.7 million men and women who have served in the wars in Iraq and Afghanistan, an estimated 20% have PTSD. Research shows that suicide risk is higher in veterans with PTSD. Tragically, more soldiers committed suicide in 2012 than the number of soldiers who were killed in combat in Afghanistan that year.
"It is critical to have an objective test to confirm PTSD diagnosis as self reports can be unreliable," says co-author Charles Marmar, MD, the Lucius N. Littauer Professor of Psychiatry and chair of NYU Langone’s Department of Psychiatry. Dr. Marmar, a nationally recognized expert on trauma and stress among veterans, heads The Steven and Alexandra Cohen Veterans Center for the Study of Post-Traumatic Stress and Traumatic Brain Injury at NYU Langone Medical Center.
The study, led by Xiaodan Yan, a research fellow at NYU School of Medicine, examined “spontaneous” or “resting” brain activity in 104 veterans of combat from the Iraq and Afghanistan wars using functional MRI, which measures blood-oxygen levels in the brain. The researchers found that spontaneous brain activity in the amygdala, a key structure in the brain’s “fear circuitry” that processes fearful and anxious emotions, was significantly higher in the 52 combat veterans with PTSD than in the 52 combat veterans without PTSD. The PTSD group also showed elevated brain activity in the anterior insula, a brain region that regulates sensitivity to pain and negative emotions.
Moreover, the PTSD group had lower activity in the precuneus, a structure tucked between the brain’s two hemispheres that helps integrate information from the past and future, especially when the mind is wandering or disengaged from active thought. Decreased activity in the precuneus correlates with more severe “re-experiencing” symptoms—that is, when victims re-experience trauma over and over again through flashbacks, nightmares and frightening thoughts.
Repeat Brain Injury Raises Soldiers’ Suicide Risk
People in the military who suffer more than one mild traumatic brain injury face a significantly higher risk of suicide, according to research by the National Center for Veterans Studies at the University of Utah.
A survey of 161 military personnel who were stationed in Iraq and evaluated for a possible traumatic brain injury – also known as TBI – showed that the risk for suicidal thoughts or behaviors increased not only in the short term, as measured during the past 12 months, but during the individual’s lifetime.
The risk of suicidal thoughts increased significantly with the number of TBIs, even when controlling for other psychological factors, the researchers say in a paper published online Wednesday, May 15 in JAMA Psychiatry, a specialty journal of the American Medical Association.
“Up to now, no one has been able to say if multiple TBIs, which are common among combat veterans, are associated with higher suicide risk or not,” says the study’s lead author, Craig J. Bryan, assistant professor of psychology at the University of Utah and associate director of the National Center for Veterans Studies. “This study suggests they are, and it provides valuable information for professionals treating wounded combat servicemen and women to help manage the risk of suicide.”
Results showed that one in five patients (21.7 percent) who had ever sustained more than one TBI reported suicidal ideation – thoughts about or preoccupation with suicide – at any time in the past. For patients who had received one TBI, 6.9 percent reported having suicidal thoughts, and zero percent for those with no TBIs. In evaluating the lifetime risk, patients were asked if they had ever experienced suicidal thoughts and behaviors up to the point they were assessed.
The increases were similar for suicidal thoughts during the previous year rather than at any time: 12 percent of those with multiple TBIs had entertained suicidal ideas during the past year, compared with 3.4 percent with one TBI and zero percent for no TBIs.
In this study, suicidal ideation was used as the indicator of suicide risk because too few patients reported a history of suicide plan or had made a suicide attempt for statistically valid conclusions to be made.
Researchers found that multiple TBIs also were associated with a significant increase in other psychological symptoms already tied to single traumatic head injuries, including depression, post-traumatic stress disorder or PTSD, and the severity of the concussive symptoms. However, only the increase in depression severity predicted an increased suicide risk.
“That head injury and resulting psychological effects increase the risk of suicide is not new,” says Bryan. “But knowing that repetitive TBIs may make patients even more vulnerable provides new insight for attending to military personnel over the long-term, particularly when they are experiencing added emotional distress in their lives.”
How the Study was Conducted
During a six-month period in 2009, 161 patients who received a suspected brain injury while on duty in Iraq were referred to an outpatient TBI clinic at a combat support hospital there. Patients were predominantly male, average age of 27, with 6.5 years of military service.
Diagnosis of traumatic brain injury was made by a clinical psychologist specifically trained in the assessment, diagnosis and management of the condition. Only patients with mild or no TBI completed all assessments; patients with moderate to severe TBI were immediately evacuated from Iraq.
TBI was confirmed if at least one clinical event was newly presented or worsened following the injury: loss of consciousness or memory, alteration of mental state, some neurological decline or brain damage.
Patients were divided into three groups based the total number of TBIs during their entire lives – zero, single TBI and two or more – the most recent of which was typically within the days immediately preceding their evaluation and inclusion in the study.
Each individual was also given surveys as part of his or her evaluation and treatment. Using standard evaluation tools, patients were surveyed about their symptoms of depression, PTSD and concussions, and their suicidal thoughts and behaviors.
“An important feature of the study is that by being on the ground in Iraq, we were able to compile a unique data set on active military personnel and head injury,” Bryan says. “We collected data on a large number of service members within two days of impact.”
At the same time, because the results of this study are based on a single clinical sample –active military in a war zone within days of the injury – the researchers note that caution is advised before assuming that the results from this particular group will apply to every other group. Studies with larger sample sizes and conducted over longer periods of time will be needed.
Why TBI is of Concern for Military Personnel
As defined by the Centers for Disease Control and Prevention, a traumatic brain injury is caused by a bump, blow or jolt to the head, or a penetrating head injury that disrupts the normal function of the brain. Effects can be mild to severe. The majority of TBIs that occur each year are concussions or other mild forms.
TBI is considered a “signature injury” of the Iraq and Afghanistan conflicts and is of particular concern because of the frequency of concussive injuries from explosions and other combat-related incidents. Estimated prevalence of TBI for those deployed in these two countries ranges from 8 percent to 20 percent, according to a 2008 study.
In addition, according to studies by the RAND Corp., suicide is the second-leading cause of death among U.S. military personnel, and the rate has risen steadily since the conflicts began in Iraq and Afghanistan. Prevalence of PTSD, depression and substance abuse have risen as well, especially among those in combat, and each has been shown to increase risk for suicidal behaviors.
“Being aware of the number of a patient’s head injuries and the interrelation with depression and other psychological symptoms may help us better understand, and thus moderate, the risk of suicide over time,” Bryan says. “Ultimately, we would like to know why people do not kill themselves. Despite facing similar issues and circumstances, some people recover. Understanding that is the real goal.”