Memory and amnesia.

Abstract

Brain damage can cause several distinct disorders of explicit memory as well as several disorders of implicit memory. Organic amnesia is the best studied explicit memory disorder. It is a syndrome that can be caused by lesions in (a) the medial temporal lobes, (b) the midline diencephalon, or (c) the basal forebrain. It remains unresolved whether one or several functional deficits underlie the syndrome, how these deficits should be characterised, and what is the exact location of the causal lesions. There is good evidence that amnesics encode information normally so their deficit(s) must be of storage or retrieval processes. If storage is disrupted, then one would expect item-specific implicit memory for certain kinds of novel information to be disrupted in amnesics. Current evidence is unable to indicate conclusively whether or not this prediction is met mainly because indirect memory test performance depends on explicit as well as implicit memory. Storage deficits should also result in accelerated forgetting in amnesic patients. Studies are described which reveal accelerated loss of free recall, but not recognition, for stories and semantically organised word lists in amnesics at delays between 15 s and 10 min. This suggests that amnesia involves a storage deficit for complex contextual associations that possibly occurs in conjunction with one or more other functional deficits.