Development of an amygdalocentric neurocircuitry-reactive aggression theoretical model of emergence delirium in posttraumatic stress disorder: an integrative literature review.

The purposes of this integrative literature review were to (1) present a synopsis of current literature describing posttraumatic stress disorder (PTSD), the amygdalocentric neurocircuitry, emergence delirium, reactive aggression, and the interaction of general anesthetics and the amygdalocentric neurocircuitry; (2) synthesize this evidence; and (3) develop a new theoretical model that can be tested in future research studies. Over the past decade, a dramatic rise in PTSD among veterans has been reported because of recent combat deployments. Modern anesthetics alter the function of the amygdalocentric neurocircuitry to produce amnesia and sedation. The etiology of emergence delirium is poorly understood, and the condition is uncommon outside the pediatric population. Emergence delirium among patients with PTSD, however, has been reported by military nurse anesthetists. To date, there have been no scientific studies conducted to identify the cause of emergence delirium in combat veterans with PTSD. This new theoretical model may explain why noxious stimuli at the time of emergence may stimulate the thalamus, leading to activation of an uninhibited amygdalocentric neurocircuitry. Because of the loss of top-down inhibition, the hyperactive amygdala then stimulates the hypothalamus, which is responsible for creating an increase in excitatory activity in the unconscious patient, resulting in emergence delirium.