The neurology of traumatic "dissociative" amnesia: commentary and literature review.

BACKGROUND

The relationship between traumatic emotional stress, hippocampal injury, memory loss, and traumatic ("dissociative") amnesia was examined.

METHOD: A survey of the research on emotional trauma, learning, memory loss, glucocosteroid stress hormones, and the hippocampus was conducted, and animal and human studies were reviewed.

RESULTS

It is well documented and has been experimentally demonstrated in animals and humans that prolonged and high levels of stress, fear, and arousal commonly induce learning deficits and memory loss ranging from the minimal to the profound. As stress and arousal levels dramatically increase, learning and memory deteriorate in accordance with the classic inverse U-shaped curve. These memory deficits are due to disturbances in hippocampal activation and arousal, and the corticosteroid secretion which can suppress neural activity associated with learning and memory and induce hippocampal atrophy. Risk and predisposing factors include a history of previous emotional trauma or neurological injury involving the temporal lobe and hippocampus, the repetitive and prolonged nature of the trauma, and age and individual differences in baseline arousal and level of cortisol.

CONCLUSIONS

Although some victims may be unable to forget, amnesia or partial memory loss is not uncommon following severe stress and emotional trauma. Even well publicized national traumas may induce significant forgetting. Memory loss is a consequence of glucocosteroids and stress-induced disturbances involving the hippocampus, a structure which normally plays an important role in the storage of various events in long-term memory.