Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
7296084 | International Journal of Psychophysiology | 2010 | 6 Pages |
Abstract
The concept of a 'fear network', i.e. an interconnected set of neural representations has been instrumental in explaining symptoms and their maintenance in anxiety disorders. The neural representations include both, response propositions such as flight or freezing and chunks of memory, conceptualized as Hebbian cell assemblies. Consequently, the fear network undergoes neuroplastic modifications, for instance, incremental enlargements with repeated exposure to threat and danger. This will in turn modify future processing of sensory stimuli and ultimately lead to an altered architecture of the brain's processing machinery and information processing modes. Using repeated exposure to traumatic stress as a model to study these processes, we summarize a series of magnetoencephalographic investigations from our laboratory, which demonstrate a characteristic pattern of early activation (before 100Â ms latency to the eliciting stimulus) in fronto-cortical circuits by high-arousing, aversive pictorial and verbal stimuli in individuals presenting with posttraumatic stress disorder (PTSD). We propose that this pattern reflects a preference of stressed brains to engage a 'low road' sensory processing, which is fast but uncoupled from prefrontal regulatory control and which easily activates an alarm response, whereas less emphasis is given the more careful and contextual processing via the 'high road' along the ventral stream. As a result, the brain's architecture is changed from a careful analyzer of the environment to a rapid threat detector with a low threshold to engage in costly defense.
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Authors
Brigitte Rockstroh, Thomas Elbert,