Post Traumatic Stress Disorder Newsletter
August 2011

This is the first Napier Counselling newsletter. I will provide you with information about a particular mental health topic in each Issue. In this issue I focus on recent research on Post Traumatic Stress Disorder (PTSD). I treat PTSD with CBT; stress management and effective visualisation techniques. The goal of treatment is to move the sensory memory of the event from the amygdala to long term memory. I am registered as a provider of mental health counselling for the PHO. The following research summary is from The US National Institute of Mental Health (NIMH) PTSD Fact Sheet.

 

Fran Lowe, PhD, Registered Psychologist

 

PTSD Introduction

 

Post-traumatic stress disorder (PTSD) is an anxiety disorder that can develop after seeing or living through an event that caused or threatened serious harm or death. Symptoms include flashbacks or bad dreams, emotional numbness, intense guilt or worry, angry outbursts, feeling "on edge," or avoiding thoughts and situations that remind them of the trauma. In PTSD, these symptoms last at least one month.

Research on Possible Risk Factors for PTSD

 

Currently, many scientists are focusing on genes that play a role in creating fear memories. Understanding how fear memories are created may help to refine or find new interventions for reducing the symptoms of PTSD. For example, PTSD researchers have pinpointed genes that make:

  • Stathmin, a protein needed to form fear memories. In one study, mice that did not make stathmin were less likely than normal mice to "freeze," a natural, protective response to danger, after being exposed to a fearful experience. They also showed less innate fear by exploring open spaces more willingly than normal mice.1

  • GRP (gastrin-releasing peptide), a signaling chemical in the brain released during emotional events. In mice, GRP seems to help control the fear response, and lack of GRP may lead to the creation of greater and more lasting memories of fear.2

Researchers have also found a version of the 5-HTTLPR gene, which controls levels of serotonin - a brain chemical related to mood-that appears to fuel the fear response.3 Like other mental disorders, it is likely that many genes with small effects are at work in PTSD.

Studying parts of the brain involved in dealing with fear and stress also helps researchers to better understand possible causes of PTSD. One such brain structure is the amygdala, known for its role in emotion, learning, and memory. The amygdala appears to be active in fear acquisition, or learning to fear an event (such as touching a hot stove), as well as in the early stages of fear extinction, or learning not to fear.4

Storing extinction memories and dampening the original fear response appears to involve the prefrontal cortex (PFC) area of the brain,4 involved in tasks such as decision-making, problem-solving, and judgment. Certain areas of the PFC play slightly different roles. For example, when it deems a source of stress controllable, the medial PFC suppresses the amygdala an alarm center deep in the brainstem and controls the stress response.5 The ventromedial PFC helps sustain long-term extinction of fearful memories, and the size of this brain area may affect its ability to do so.6

Individual differences in these genes or brain areas may only set the stage for PTSD without actually causing symptoms. Environmental factors, such as childhood trauma, head injury, or a history of mental illness, may further increase a person's risk by affecting the early growth of the brain.7 Also, personality and cognitive factors, such as optimism and the tendency to view challenges in a positive or negative way, as well as social factors, such as the availability and use of social support, appear to influence how people adjust to trauma.8 More research may show what combinations of these or perhaps other factors could be used someday to predict who will develop PTSD following a traumatic event.

Psychotherapy Treatment

 

Cognitive behavioral therapy (CBT) teaches different ways of thinking and reacting to the frightening events that trigger PTSD symptoms and can help bring those symptoms under control. There are several types of CBT, including exposure therapy, cognitive restructuring, and stress inoculation training.

NIMH is currently studying how the brain responds to CBT compared to sertraline (Setrona) for treating PTSD. This research may help clarify why some people respond well to medication and others to psychotherapy

Treatment Medications

 

In a small study, NIMH researchers recently found that for people already taking a bedtime dose of the medication prazosin (Apo-Prazo), adding a daytime dose helped to reduce overall PTSD symptom severity, as well as stressful responses to trauma reminders.9

Another medication of interest is D-cycloserine, which boosts the activity of the neurotransmitter NMDA, which is needed for fear extinction. In a study of 28 people with a fear of heights, scientists found that those treated with D-cycloserine before exposure therapy showed reduced fear during the therapy sessions compared to those who did not receive the drug.10 Researchers are currently studying the effects of using D-cycloserine with therapy to treat PTSD.

Propranolol (Angilol), a beta-blocker, is also being studied to see if it may help reduce stress following a traumatic event and interrupt the creation of fearful memories. Early studies have successfully reduced or seemingly prevented PTSD in small numbers of trauma victims.11

References

 

1. Shumyatsky GP, Malleret G, Shin RM, et al. stathmin, a Gene Enriched in the Amygdala, Controls Both Learned and Innate Fear. Cell. Nov 18 2005;123(4):697-709.

2. Shumyatsky GP, Tsvetkov E, Malleret G, et al. Identification of a signaling network in lateral nucleus of amygdala important for inhibiting memory specifically related to learned fear. Cell. Dec 13 2002;111(6):905-918.

3. Hariri AR, Mattay VS, Tessitore A, et al. Serotonin transporter genetic variation and the response of the human amygdala. Science. Jul 19 2002;297(5580):400-403.

4. Milad MR, Quirk GJ. Neurons in medial prefrontal cortex signal memory for fear extinction. Nature. Nov 7 2002;420(6911):70-74.

5. Amat J, Baratta MV, Paul E, Bland ST, Watkins LR, Maier SF. Medial prefrontal cortex determines how stressor controllability affects behavior and dorsal raphe nucleus. Nat Neurosci. Mar 2005;8(3):365-371.

6. Milad MR, Quinn BT, Pitman RK, Orr SP, Fischl B, Rauch SL. Thickness of ventromedial prefrontal cortex in humans is correlated with extinction memory. Proc Natl Acad Sci U S A. Jul 26 2005;102(30):10706-10711.

7. Gurvits TV, Gilbertson MW, Lasko NB, et al. Neurologic soft signs in chronic posttraumatic stress disorder. Arch Gen Psychiatry. Feb 2000;57(2):181-186.

8. Brewin CR. Risk factor effect sizes in PTSD: what this means for intervention. J Trauma Dissociation. 2005;6(2):123-130.

9. Taylor FB, Lowe K, Thompson C, et al. Daytime Prazosin Reduces Psychological Distress to Trauma Specific Cues in Civilian Trauma Posttraumatic Stress Disorder. Biol Psychiatry. Feb 3 2006.

10. Ressler KJ, Rothbaum BO, Tannenbaum L, et al. Cognitive enhancers as adjuncts to psychotherapy: use of D-cycloserine in phobic individuals to facilitate extinction of fear. Arch Gen Psychiatry. Nov 2004;61(11):1136-1144.

11. Pitman RK, Sanders KM, Zusman RM, et al. Pilot study of secondary prevention of posttraumatic stress disorder with propranolol. Biol Psychiatry. Jan 15 2002;51(2):189-192.

If you do not wish to receive this newsletter, please phone 021 055 4897 or email Fran@napiercounselling.co.nz