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Also involved in the fear reaction is the amygdala, the emotional hub of our brain, which regulates not just fear but also anger, pleasure, desire and more. In a series of experiments that investigated how mice who were fearful reacted to being startled, Davis showed that while anxiety may be related to fear, it is a more prolonged and diffuse response that involves a broader network of brain circuits.
That makes sense, since anxiety is not just a fear of imminent danger but also a broader prospective reaction to possible dangers. This plays a critical role in certain types of clinical anxiety such as phobias, panic attacks and PTSD that are often consequences of having lived through or learned about a threatening experience--and coming to dread its recurrence. Awful as that is to go through, it's also highly adaptive. The fight-or-flight response wouldn't be useful, after all, if we didn't learn from each near death event by making a powerful mental record of whatever signals alerted us to the impending threat--the shadow of the approaching tiger or the footsteps that once signaled a mugger and could again. People with panic disorders thus fret over what could trigger their next attack, always on the lookout for any potential catalyst that could set them off; obsessive-compulsive patients tend to focus on one possible negative outcome--being robbed, say--and compulsively work to prevent that from happening, perhaps by repeatedly checking the lock on their door.
Davis' understanding of all this led to a more sophisticated map of anxiety, which many experts now believe involves constant activation of a part of the fear response known as the hypothalamus-pituitary-adrenal (HPA) axis and failure to turn it off when a threat has passed. Keeping that signal alive may be the responsibility of the brain region known as the bed nucleus of the stria terminalis (BNST), which regulates the autonomic part of our nervous system, including heart and breathing rates, and is more active in the brains of anxiety-disorder patients. The BNST is fueled by adrenaline, which means the HPA axis, unlike the fear response, may not always involve cortisol.
Dr. James Abelson, director of the Stress & Anxiety Disorders Program at the University of Michigan, helped confirm this thinking with a study involving people who were anxious about driving and dreaded the next time they had to get behind the wheel. Measuring the cortisol in the subjects' saliva an hour before they arrived at the lab and again while they were on a test drive, he and his colleague found that the cortisol was the same despite the subjects' reporting feeling more anxious and worried while they were driving.
Learning from Fear
To patients suffering from either full-blown fear or more-pedestrian anxiety, the perfectly reasonable response to this is, So what? Why does the biological basis matter, since both conditions feel lousy no matter what? The fact is, it matters a lot. The fight-or-flight response, with its surging cortisol and respiratory and cardiovascular hysteria, leaves little room for learning, because it often bypasses the higher regions of the brain. Anxiety, by contrast, engages one more critical region of the brain--the prefrontal cortex, where we collect our thoughts by planning, organizing and reasoning.