A relatively newer paradigm for investigating neurobiological abnormalities in PTSD has emerged in the measurement of brain wave activity with a special kind of electroencephalogram (EEG) measure called event-related potentials (ERPs). Event-related potentials measure changes in EEG activity in response to stimuli and serve as indices of reactivity and habituation and learning against background resting-state activity. An ERP, for example, serves as a measure of the brain's reaction to novel stimuli, with a reduction in activity as information is habituated to and is deemed repetitive or noninformative.
Arciniegas and colleagues (2000) have proposed that the symptoms of hyper-vigilance and attention deficits in PTSD are consequences of a reduction in sensory gating. Boutros and Belger (1999) define sensory gating as follows:
[T]he ability of the brain to modulate its sensitivity to incoming sensory stimuli. This definition allows the concept of gating to include both the capacities to minimize or stop responding to incoming irrelevant stimuli (gating out) and to respond when a novel stimulus is presented or a change occurs in ongoing stimuli (gating in). (p. 917, abstract)
Metzger, Gilbertson, and Orr (2005) propose that in PTSD, selective attention is impaired because of a failure to filter out irrelevant environmental stimuli. They state, "Instead, they [PTSD sufferers] interpret or respond to repetitive stimuli as though they might maintain some significance." In other words, all stimuli are considered potentially relevant and, perhaps, dangerous because of their novelty.
Other researchers have found that not only do PTSD sufferers respond to a broader range of stimuli as novel for a longer period of time, but they also have an increased sensitivity to stimulus intensity. Under normal conditions and functioning, there is an increase in brain response with corresponding increases in stimulus intensity. But if the stimulus is too intense, there should be a smaller, more circumscribed brain response. This is viewed as a protective mechanism against overstimulation. In PTSD, this protective mechanism is engaged at lower stimulus thresholds than for non-PTSD sufferers. This research suggests rather direct biological evidence for the phenomenon of reactivity in PTSD.
Finally, in addition to poor habituation and lowered thresholds, researchers have found heightened sensitivity to stimulus change and novelty. Event-related potentials sensitive to this process have shown that in PTSD this process is amplified, leading to increased sensitivity to novelty and monopolization of attention resources.
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