You can never completely abolish a learned fear, says Pitman. Learned fears are deep and may strengthen by reconsolidating after recall. One way to help patients diminish the impact of an anxiety-producing memory is to guide them to form a new memory that inhibits, or extinguishes, expression of the fearful memory during any recall attempt.
Or, as Pitman and colleagues discovered several years ago, people might be helped to stave off a fear-filled memory by preventing it from consolidating in the first place. In a controlled study of patients entering Mass General's emergency department after traumatic experiences-assaults or car accidents, for example-Pitman provided some participants with a placebo and others with propranolol, a drug that blocks the effects of the hormone adrenaline. At follow-up interviews participants listened to audiotapes of their own accounts of their trauma the day it occurred. Propranolol recipients had weaker physical responses to the tapes than placebo users, who showed physical signs of the stirring of their fearful memory despite time's passage.
Replicating these results has proven difficult, however, so Pitman and colleagues have shifted their focus to reactivating traumatic memories in people with post-traumatic stress disorder and then administering an anti-stress drug to try to weaken the memory's reconsolidation.
Reliving a fear, even a trauma-induced one, is not necessarily pathologic, Milad points out. Recalling the source of high emotion or injury can serve as a safeguard, a warning that our brains can tap as needed. In addition, time often softens the intensity of response.
Say you're in a car accident, Milad adds. It occurs at a particular intersection at the same time a certain song is playing on the radio. For a period following that accident, whenever you go through that intersection or hear that song, you will re-experience at some level your initial fear. If over time nothing horrible happens to rekindle your memory, your conditioned response to either stimulus will lessen until the fear is extinguished. This extinction doesn't erase the initial learned fear; instead, it leads to forming a new memory, a 'safety memory.' The learned fear-the neuronal connections that the experience formed within your amygdala and between your amygdala and certain cortical structures-remains.
For some, the trauma never lessens. In people with post-traumatic stress disorder, Milad and Pitman have found that two brain regions involved in extinction, the hippocampus and a region of the prefrontal cortex, function at a lesser capacity, while activity in the amygdala and the dorsal anterior cingulate, a region involved in cognition and motor control, rachets up. These findings may explain the unending rawness that trauma-induced fears bring to people with the disorder.
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