Traumatic amnesia, repression, and hippocampus injury due to emotional stress, corticosteroids and enkephalins.
The role of stress, arousal, emotional trauma, and corticosteroid and enkephalin secretion on memory and the hippocampus, and the development of traumatic amnesia and repressed memory syndrome are detailed. Animal and human studies are reviewed. Trauma-induced memory deficits appear to be secondary to abnormal neocortical and hippocampal arousal, and corticosteroid and enkephalin secretion which can induce atrophy or seizures within the hippocampus, suppress hippocampal theta activity and long term potentiation, as well as injure hippocampal pyramidal cells. Predisposing factors include individual, age, and sex differences in arousal, and previous emotional trauma or temporal lobe or hippocampal injury. However, as the amygdala processes and stores emotional experiences in memory, patients may also demonstrate trauma related symptoms, including flashbacks as well as shrinking retrograde amnesia.
Joseph
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Brain Research Laboratory, San Jose, CA 95126, USA.
D000305:Adrenal Cortex Hormones / Q000378:metabolism*; D000328:Adult; D000647:Amnesia / Q000209:etiology* / Q000503:physiopathology / Q000523:psychology; D002648:Child; D002650:Child Abuse, Sexual / Q000523:psychology; D002675:Child, Preschool; D004745:Enkephalins / Q000378:metabolism*; D005260:Female; D006624:Hippocampus / Q000293:injuries* / Q000503:physiopathology; D006801:Humans; D007223:Infant; D008297:Male; D012094:Repression, Psychology; D013313:Stress Disorders, Post-Traumatic / Q000503:physiopathology
D000305:Adrenal Cortex Hormones; D004745:Enkephalins