Biological Mechanisms Of

Biological perspectives have focused on fear conditioning and progressive neural sensitization in the weeks after trauma as possible explanations of the genesis of PTSD (Kolb, 1987; Pitman, Shalev, & Orr, 2000). It is possible that sensitization occurs as a result of repetitive activation by trauma reminders, which elevate sensitivity of limbic networks (Post, Weiss, & Smith, 1995), and that as time progresses these responses become increasingly conditioned to trauma-related stimuli (LeDoux, Iwata, Cicchetti, & Reis, 1988). In support of these proposals, there is evidence that people who eventually develop PTSD display elevated resting heart rates in the initial week after trauma (Bryant, Harvey, Guthrie, & Moulds, 2000b; Shalev et al., 1998; see also Blanchard, Hickling, Gaslovski, & Veazey, 2002). There is also evidence that lower cortisol levels shortly after trauma predict subsequent PTSD (McFarlane, Atchison, & Yehuda, 1997; Delahanty, Raimonde, & Spoonster, 2000). Cortisol may act as an "anti-stress" hormone that restores equilibrium, and lower cortisol levels may reflect an incapacity to lower arousal following trauma (Yehuda, 1997). The importance of increased arousal in the acute phase is also indicated by the prevalence of panic attacks in people with ASD (Bryant & Panasetis, 2001; Nixon & Bryant, 2003). A promising finding emerged from a pilot study that attempted to prevent PTSD by administering propranolol (a beta-adrenergic blocker) within 6 hours of trauma exposure (Pitman et al., 2002); there is evidence that propanolol abolishes the epinephrine enhancement of conditioning (Cahill, Prins, Weber, & McGaugh, 1994). Although propanolol did not result in reduced PTSD relative to a placebo condition, patients receiving propanolol displayed less reactivity to trauma reminders 3 months later. A subsequent study has found that propanolol administered immediately after trauma does reduce PTSD severity 2 months later (Vaiva et al., 2003). This outcome suggests that propanolol administration shortly after trauma exposure may limit the fear conditioning that may contribute to subsequent PTSD development.

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