Central Oregon's Chief Pediatric Counseling Clinic
Derick E. Vergne, MD.
September 24, 2014
Extreme terror is an advantageous evolutionary emotion designed for protection against real danger by prompting the person experiencing it either to fight or to flee. This classic “fight or flight” response is basically one and the same, with self-preservation as the common denominator.
Once the potential danger disappears, the experience of fear and terror is no longer needed, yet it may persist. In fact, continuous fear (when no longer needed to survive) becomes disadvantageous to the organism, because these feelings will prevent it from effectively looking for food and shelter, thereby threatening its very survival.
The abnormal psychological and physical experience of fear in safe or neutral situations long after the initial traumatic experience has passed is diagnosed as post-traumatic stress disorder (PTSD), or anxiety disorder. Variants in the quality and timing of the experience of danger lead to diverging diagnoses as generalized anxiety and phobias. The question is, how is experience turned into physiology—or more accurately, what are the neurobiological underpinnings of fear, and how are those activated by experience?
The amygdala is a well-known epicenter for the emotional “understanding” of stimuli. In other words, the amygdala helps the brain to remember the averseness of otherwise neutral stimuli. Therefore, the amygdala is an integral part of the circuitry maintaining memories for aversive events.
An increasing amount of research in recent years has been geared toward defining circuitry and neurotransmitter abnormalities in patients with anxiety disorders, be it generalized anxiety or PTSD. Clinical studies based on animal data consistently point to amygdala hyperactivity in anxiety disorders.
To better grasp the extent to which the amygdala relates to fear and the stress response, it is much easier to think about the fight-or-flight mechanism. For instance, when the zebra notices the staring lion—or the human notices the approaching deadline, accompanied by a frowning, angry boss—the amygdala is immediately activated, followed by hypothalamus stimulation of the pituitary, ultimately causing the adrenal glands to secrete cortisol (the classic stress hormone). Cortisol induces release of the stress neurotransmitters norepinephrine and adrenaline, with the accompanying sympathetic (elevated heart rate, tremors, pounding heart, and slow digestion) and psychological (fear, apprehension) changes.
Although further discussion is beyond the scope of this article, the extrahypothalamic stress axis is another way in which brain uses norepinephrine through the amygdala, bypassing pituitary and adrenal cortisol. The extra-hypothalamic stress axis is purported to be important in the perpetuation of the stress response and its psychological sequela, anxiety. The amygdala is therefore a key component of the stress response.
What differentiates the generally calm individual from the chronically anxious person is not necessarily that one has “high” vs “low” amygdala function, but specifically the way in which the amygdala communicates with the “thinking part” of the brain. How does the brain think it through to modulate its activity? Research is now concentrated on clarifying how the prefrontal cortex (thinking brain) and the amygdala (primitive fear structure) communicate to modulate anxious states. Clinical neuroimaging studies have begun to clarify the neuroanatomical and neurochemical relationship between the prefrontal cortex and amygdala in the regulation of the stress response and anxious states.
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