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    1999), disturbances of serotonergic activity (stress resilience, sleep regulation, impulse control, conditioned avoidance, and aggression), and viagra death lawsuit kindling (lowering of the excitability threshold after repeated electrical stimulation). After traumatic exposure, limbic nuclei become sensitized, leading to excessive 506 Psychological Aspects of Women’s Health Care, Second Edition responsivity and increased startle and arousal responses—cores feature of PTSD that often persist after other symptoms resolve. These include noradrenergic dysregulation (increased sensitivity of the sympathetic nervous system under stress) (Southwick et al. Activation of the amygdala is postulated to mediate the autonomic stimulation resulting from exposure to trauma, thus transforming sensory input into physiologic signals that, in turn, produce and modulate emotional responses.

    As van der Kolk (1997) has described, people with PTSD develop significant alterations in physiologic reactivity and stress hormone secretion, making it difficult to “properly evaluate sensory stimuli and respond with appropriate levels of physiologic and neurohormonal arousal.” Several psychophysiologic models have been posited to explain PTSD (Davidson and van der Kolk 1994).