Amnesic Disorders

Abstract During the past five decades, our understanding of disorders of memory and of normal memory processes has increased dramatically. In 1950, very little was known about the localization of brain lesions causing amnesia. Despite a few clues in earlier literature, it came as a complete surprise in the early 1950s that bilateral medial temporal resection caused amnesia. The importance of the thalamus in memory was hardly suspected until the 1970s and the basal forebrain was an area virtually unknown to clinicians before the 1980s. An animal model of the amnesic syndrome was not developed until the 1970s. During this same period, neuropsychological characteristics of amnesia were being un- covered through intense research efforts with clinical populations. The amnesic syndrome has been a topic of fundamental interest to neuropsychologists, neuroscientists, and cognitive psychologists (Baddeley, 1982); the resulting literature in many respects reflects a model system for the interdisciplinary activity that some refer to as “cognitive neuropsychology” (Caramazza, 1992; Kosslyn and Intriligator, 1992) or “cognitive neuroscience” (Kosslyn and Koenig, 1992; Schacter et al., 1998). As a result of this explosion of activity, we no longer consider memory to be a unitary phenomenon.