Thursday, February 23, 2012

Anxiety News Stories

Veterans Receive Evaluation for PTSD

Sunday, 13 February 2011 16:33 Written by Administrator

Joan Cook, Ph.D., of Yale University and colleagues have been awarded funds from the American Recovery and Reinvestment Act of 2009 to evaluate the implementation of two evidence-based psychotherapies for treating post traumatic stress disorder (PTSD) among veterans. The grant addresses the NIH Challenge Grant topic "Strategies to Support Uptake of Interventions within Clinical Community and Settings."

Strategies for promoting evidence-based PTSD treatments in the military are urgently needed as more and more soldiers returning from Iraq and Afghanistan struggle with this disorder. The research team will characterize and assess the implementation of two types of therapy—prolonged exposure (PE) therapy and cognitive processing therapy (CPT)—within the U.S. Department of Veterans Affairs (VA) residential PTSD treatment programs. PE involves helping people confront their fear and feelings about the trauma they experienced in a safe way through mental imagery, writing, or other ways. In CPT, the patient is asked to recount his or her traumatic experience, and a therapist helps the patient redirect inaccurate or destructive thoughts about the experience.

Dr. Cook and colleagues will partner with the Northeast Program Evaluation Center, which monitors all VA mental health programming and patient outcomes, and the National Center for PTSD, which oversees the dissemination of PE and CPT nationally among VA providers. They plan to monitor and assess the efforts of more than 250 mental health providers in residential PTSD treatment settings via online questionnaires, semi-structured interviews, and on-site observations. The researchers note that the project may help improve the dissemination of other evidence-based treatments in federally-funded mental health systems.

The NIH Challenge Grants in Health and Science Research program is a new initiative funded through the American Recovery and Reinvestment Act of 2009 (Recovery Act). This program will support research on 15 broad Challenge Areas that address specific scientific and health research challenges in biomedical and behavioral research that would benefit from an influx of significant two-year funds to quickly advance the area.

Within these Challenge Areas, NIMH has identified 35 topics of particular funding interest that will advance the Institute's mission and the objectives outlined in the NIMH Strategic Plan, the Trans-NIH Plan for HIV-Related Research, and the National Advisory Mental Health Council report on research training. These topics can be found at NIMH's Challenge Grant web page.

Source: www.nimh.nih.gov/index.shtm

Hormone Linked to Panic Attacks

Sunday, 13 February 2011 16:31 Written by Administrator

Science Update
December 28, 2009

Runaway Vigilance Hormone Linked to Panic Attacks

Translational Experiments in Rats, Humans Suggest New Medication Target

A study has linked panic disorder to a wayward hormone in a brain circuit that regulates vigilance. While too little of the hormone, called orexin, is known to underlie narcolepsy, the new study suggests that too much of it may lead to panic attacks that afflict 6 million American adults.

"Targeting the brain's orexin system may hold promise for a new generation of anti-anxiety treatments," said Thomas R. Insel, M.D., Director of the National Institute of Mental Health (NIMH), part of the National Institutes of Health. "This is a good example of how translational experiments in rats and humans can potentially yield clinical benefits."NIMH grantee Anantha Shekhar, M.B., Ph.D., and colleagues at Indiana University and Lund University, report on their findings online Dec. 27, 2009 in the journal Nature Medicine. They showed that blocking orexin gene expression or its receptor prevented panic attack-like responses in rats. The study also revealed that panic disorder patients have excess levels of the hormone.

Background
Orexin, also called hypocretin, is secreted exclusively in a circuit emanating from the brain's hypothalamus, known to regulate arousal, wakefulness and reward.Panic attacks can be experimentally-induced by infusing susceptible humans with a normally innocuous salt called sodium lactate. The salt similarly triggers panic-like anxiety behaviors in susceptible rat strains, suggesting that something is altered in their arousal circuit. Since sodium lactate activated orexin-secreting neurons in panic-prone rats but not in control rats, the researchers hypothesized that something might be orexin.

Results of This Study
The investigators first discovered that increased gene expression in orexin-secreting neurons correlated with increases in anxiety-like behavior in panic-prone rats following sodium lactate infusions. Using a technique called RNA interference, they then protected the panic-prone rats from developing anxiety behaviors following the infusions by first injecting them with a genetically-engineered agent that prevented orexin genes from turning on. Blocking orexin receptors with a drug that specifically binds to it also blocked the anxiety like behavior following the infusions. This mirrored effects, seen in both rats and humans, of benzodiazepine medications used to treat panic disorder.

The excess sleepiness of narcolepsy, traced a decade ago to loss of orexin-secreting neurons in the arousal circuit, might seem to be an opposite state of a panic attack. However, the researchers demonstrated in rats that such sedation could not account for orexin's effects on anxiety. Also in rats, they traced orexin neurons to their end target to pinpoint the specific brain site that accounts for the anxiety effects, disentangled from cardio-respiratory components of the panic response.

Finally, by measuring orexin in cerebrospinal fluid of 53 patients, the researchers showed that those with just panic disorder had higher levels of orexin than those with both panic disorder and depression.

Significance
Taken together, these results and other evidence suggest a critical role for an overactive orexin system in producing panic attacks, say the researchers.

What's Next?
Medications that block the orexin receptor may provide a new therapeutic approach for the treatment of panic disorder, they add.

The research was also supported, in part, by NIH's National Center for Research Resources.

Reference
A key role for orexin in panic anxiety. Johnson PL, Truitt W, Fitz SD, Kelley PE, Dietrich A, Sanghani S, Traskman-Bendz L, Goddard AW, Brundin, L, Shekhar A. Nature Medicine. Epub 2009 Dec 27.

Source: http://www.nimh.nih.gov/index.shtml

Anxious, Depressed Teens, Adults Reactions Differ

Sunday, 13 February 2011 16:29 Written by Administrator

Brain Reactions DifferScience Update
December 02, 2008

Anxious and Depressed Teens and Adults: Same Version of Mood Gene, Different Brain Reactions

An NIMH study using brain imaging shows that some anxious and depressed adolescents react differently from adult patients when looking at frightful faces. This difference occurs even though the adolescent and adult patients have the same version of a mood gene. Researchers in the NIMH Mood and Anxiety Disorders Program and colleagues reported these findings online October 31, 2008, in the journal Biological Psychiatry.

Background
Anxiety and depression are influenced by the processing of the mood-regulating brain chemical called serotonin. A protein known as the serotonin transporter directs serotonin from the space between nerve cells back into the cells, where it can be reused. Changes in the gene that codes for the serotonin transporter can lead to decreased transport of serotonin back into the brain’s nerve cells. Abnormalities in the serotonin system are associated with anxiety and depression.

Everyone inherits two copies of the serotonin transporter gene—one from each parent. The gene has various versions—one version is short, and one version is long. A person may have two copies of the same version or one copy each of two different versions. Previous studies in adults have linked versions of the gene to increased risk for mood and anxiety disorders. Adults who have one copy of the short version tend to be more anxious and depressed than adults who have two copies of the long version.

Previous brain imaging studies in adults linked gene versions to different responses of the brain’s fear hub—the amygdala—to frightful faces. In both healthy and affected adults who have at least one copy of the short version, the amygdala reacts more than it does in healthy or affected adults who have two copies of the long version of the gene. Whether these findings in adults also hold true for adolescents was unknown. Using functional magnetic resonance imaging (fMRI), Jennifer Y. F. Lau, Ph.D., then at NIMH and now at the University of Oxford, U.K., and colleagues at NIH scanned the brains of 33 healthy teens and 31 teens with depression and anxiety disorders while they viewed pictures of frightful faces. Then the investigators compared the amygdala reactions in the two groups.

Findings of This Study
Lau and colleagues found that in healthy adolescents who have at least one copy of the short version of the gene, the amygdala reacts more than it does in healthy adolescents who have two copies of the long version. This result is the same in healthy adults. However, in anxious or depressed adolescents, the opposite results were found. In affected adolescents who have at least one copy of the short version, the amygdala reacts less than it does in affected adolescents who have two copies of the long version.

Significance
This finding in affected teens with two long version genes is the opposite of that observed in anxious or depressed adults. It is surprising because anxiety and depression during adolescence tend to predict these disorders during adulthood.

What’s Next?
The unexpected finding may be explained by the fact that anxious adults and anxious adolescents react differently when presented with threats. But further research is needed to fully understand the difference, the investigators say.

Reference
Lau JY, Goldman D, Buzas B, Fromm SJ, Guyer AE, Hodgkinson C, Monk CS, Nelson EE, Shen PH, Pine DS, Ernst M. Amygdala Function and 5-HTT Gene Variants in Adolescent Anxiety and Major Depressive Disorder. Biological Psychiatry. 2008 Oct 23. [Epub ahead of print].

Source: http://www.nimh.nih.gov/index.shtml