Trauma and the Brain

 

How brain systems respond to traumatic events

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In most cases, people who experience a traumatic event are able to process the situation and move forward. Other times, the brain seems to work against us with symptoms of anxiety, hypervigilance, flashbacks, or insomnia after the event. These symptoms can persist for years, and sometimes for a lifetime.

Approximately 7.8% of the population will develop post-traumatic stress disorder (PTSD) at some point in their lives. As a neuropsychologist, Dr. Curtis Cripe looks at symptoms of PTSD from the perspective of the way brain networks interact. With advances in neuroimaging techniques, researchers have been able to study and identify how the brain structures change with PTSD. Dr. Curtis Cripe pointed out that the three areas of the brain involved with PTSD include the prefrontal cortex, the amygdala, and the hippocampus. Based on neuroimaging studies, we can see that each of these brain regions are impacted in people experiencing PTSD. As these three key brain regions interact, the symptoms of PTSD develop.

Amygdala

PTSD is commonly linked to high activity in the amygdala. This is a structure in the brain that is involved with fear circuitry and the fight-flight-freeze response. In people experiencing symptoms of PTSD, Dr. Curtis Cripe noted that the amygdala goes into over-drive. It's as if this region gets stuck.

In people with PTSD, the amygdala shows a heightened, or exaggerated response to emotional input. Sometimes this may be a trauma-related stimulus, like the sound of fireworks for a combat veteran. Other times, the stimulus may be unrelated to the person's trauma experience. For people dealing with PTSD, they know the constant fear and hypervigilance that results from these exaggerated response in the amygdala.

Hippocampus

When looking further at brain imaging studies, Dr. Curtis Cripe sees reduced activity in the hippocampus. This is the region of the brain involved with placing context around fear conditioning, as well as creating memories of experiences and facts (explicit memory).

Following a traumatic event, long-term exposure to stress hormones causes cell damage in the hippocampus. As a result, the hippocampus loses volume and becomes smaller. This structural change in the brain is due to PTSD.

The hippocampus interacts directly with the amygdala to form emotional memories. As the amygdala becomes hyper-active, it exaggerates the fear response. The hippocampus becomes hypo-active, and fails to create context for emotional information. This imbalance creates an interaction between brain systems where symptoms of PTSD emerge.

Prefrontal Cortex

People who have been diagnosed with PTSD consistently show low activity in the prefrontal cortex. This brain region is involved in important cognitive functions. When looking at PTSD, the prefrontal cortex works to regulate and make sense of emotional information. This is the area of the brain that would process and extinguish learned fear conditioning.

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The amygdala is creating an exaggerated response to emotional triggers. It doesn't have the context and facts that the hippocampus would normally provide. At the same time, Dr. Curtis Cripe points out that the prefrontal cortex fails to moderate and extinguish unnecessary fear responses.

The Solution

Dr. Curtis Cripe points out that the solution is strengthening and rebalancing these key brain regions. Through targeted interventions, he is able to track progress and bring the brain back online to work in a more healthy way to respond appropriately to external input. As the brain reaches that balance, the amygdala and hippocampus are able to take in experiences and create meaningful context to understand emotional information. The prefrontal cortex is able to process those emotional memories and make decisions about when a response is no longer needed.

Dr. Curtis Cripe, Ph.D. is the director of research and development at NTL Group, Inc. F or more information on his neuroengineering approach to improving brain function with PTSD, click here.