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Memory Mechanisms in Posttraumatic Stress Disorder

Received January 16, 2001; revised June 22, 2001; accepted June 27, 2001. From the Department of Physical Medicine and Rehabilitation, MetroHealth Medical Center and Department of Psychiatry, Case Western Reserve University, Cleveland, Ohio (B.L.), and the Department of Psychiatry, University of Cincinnati, Cincinnati, Ohio (R.K.). Address correspondence to Dr. Layton, MetroHealth Medical Center, 2500 MetroHealth Drive, Cleveland, OH 44109. E-mail: blayton{at}metrohealth.org

The authors present a new theory of the neurobiological mechanisms mediating the memory processes involved in posttraumatic stress disorder (PTSD). The current fear-conditioning model accounts for learning that underlies certain central features of PTSD, but it fails to account for peritraumatic memory disturbances, episodic memory phenomena that also are characteristic of the disorder. A more comprehensive model of PTSD, consistent with the clinical phenomenology of the disorder, is proposed on the basis of observations from human memory experiments. It is argued that the amygdala is the locus of consolidation of the core of the traumatic experience and that amygdalar inhibition of hippocampal function at high levels of emotional arousal mediates diminution of conscious memory for peritraumatic events. The model is amenable to specific experimental manipulations that should yield information pertinent to further development of theory and, ultimately, to more rational clinical intervention.

Key Words: Posttraumatic Stress Disorder • Memory • Amygdala • Hippocampus

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