Bővebb ismertető
I INTRODUCTION
Disorders of memory have in the ig6os constituted one of the central subjects of research in neurology and neuropsychology. Many factors have contributed to this revival of research on amnesic disorders. Certain cases with "generalized memory loss" which have complicated surgical procedures in epilepsy have been among the most prominent causes. These were cases where the temporal lobes were extirpated bilaterally. First reports of such cases were published already in the 1950s (Scoville 1954, Terzian & Ore 1955, Scoville & Millner 1957). Apart from these "semi-experimental" brain lesions, a severe general memory disorder has been observed to be a concomitant in many other brain lesions, too. The etiology of such brain lesions may include most varied diseases, not to mention alcohol which has been known since long ago. These brain lesions have often been found to be comparatively local and restricted and situated bilaterally in the deep structures of the brain, close to its midline. More specifically, brain lesions have been found in the region of the limbic system, which is defined on a functional basis (Maclean 1952, Hassler 1964, Brodal 1969). The classic symptoms described by Korsakoff in the years 1887 to 1890, have again emerged as the subject of central interest to the study on memory. Since Korsakoff's clinical descriptions controversial opinions about the basic elements of the syndrome which consists of these symptoms have occurred. A multitude of theories have been offered to explain the syndrome. The integral basic symptom of the Korsakoff syndrome has, however, remained the same, i.e. the general widespread disorder of recent memory which manifests itself e.g. as a rapid forgetting of daily events. On the other hand, in the 1960s the so-called "limited amnesias" have separated as a particular group, different from the general memory disorder typical of the Korsakoff syndrome. These amnesias affect only a limited memory material, and, above all, it is the cortical representation areas of certain functions which have been damaged. This differentiation of memory disorders has engendered a still more thorough analysis of them. The results of these analyses have provided even the clinician with more clues to the significance of local cerebral damages.
Brain injuries are among the most common causes of clinically verified memory disorders, but, on the other hand, a brain-injured patient generally has not been regarded as an appropriate object for memory research since the