Amnesia refers to a relatively circumscribed deficit in declarative memory that cannot be accounted for by impairments in attention, language, motivation, reasoning, or other nonmnemonic abilities. It is defined by a behavioral syndrome and not by etiology or lesion location. The severity of the deficit can vary considerably, but at a minimum it interferes with daily activities and quality of life. The purity of the deficit also varies because many patients have some degree of other cognitive difficulties as well. To the extent that those difficulties are mild and do not account for the memory deficit, a patient may be classified as amnesic. Otherwise, a patient may be better classified as demented, with memory being one of multiple deficits. The amnesia is described as global if it extends to both verbal and nonverbal information. The amnesic patient performs well on tests of attention, reasoning, and general information as long as the tests do not make demands on declarative memory.
Patients with pure amnesia have a pervasive impairment on tests of declarative memory. The anterograde amnesia extends to memory for all sorts of materials and events in all modalities. It is apparent in both easy and difficult tests of memory. The severity of amnesia varies considerably, however, so that a mildly amnesic patient could perform well on easy tests of memory. Because judgment is preserved in amnesic patients, they are usually aware of having a memory problem. They may, however, underestimate the severity of the problem because they are aware only of memory difficulties at the present moment and cannot remember the sorts of memory failures they experienced earlier.
Amnesic patients perform normally on tests of immediate memory, classic conditioning, skill learning (motoric, perceptual, and cognitive), and perceptual and conceptual repetition priming.^ Declarative memory, however, is often invoked by tests that are not ostensibly memory tests. Many complex tests of cognition require some degree of declarative memory, if only to remember the instructions for the test. Other tests confound anterograde amnesia with general knowledge. For example, a patient who became amnesic in 1985 would not know the current president of the United States and other sorts of widely known information about events since 1985. For the same reason, a purely amnesic patient could even fail to answer some questions used to probe orientation, such as where the patient is at present. The amnesic patient would not remember the name or address of a hospital or medical building and would not know the day, month, or year because all of these facts are learned via declarative memory. For these reasons, intelligent amnesic patients may earn a poor score on a standard dementia rating scale. Pure amnesia is quite rare, so routine application of assessment measures may be misleading.
Amnesia by definition features an anterograde amnesia, and a retrograde loss of memories is frequently but variably present. The retrograde amnesia is typically temporally graded, with more recent memories being most vulnerable to amnesia and remote memories most likely to be spared. In general, the severity of anterograde and retrograde amnesias are correlated. If a lesion extends laterally from medial temporal lobe areas, it may injure temporal lobe regions that normally represent autobiographical knowledge. Such a lesion would exacerbate the retrograde amnesia and lead to a more extensive loss of acquired memories, even important ones from remote time periods.
Amnestic syndromes can occur in isolation or can be accompanied by other neurological signs. In patients with the Wernicke-Korsakoff syndrome (see Chapter.40 ), which is often associated with thiamine deficiency but also with head trauma, epilepsy, and anoxia, amnesia may develop in the context of ataxia and extraocular muscle pareses. An overall confusional state may be seen early in such cases, but the enduring learning and memory deficit is the most distinctive mental aberration of this syndrome. In such cases, the anatomical lesion should be sought in the diencephalon, medial temporal lobes, mamillary bodies, and connecting pathways of these regions regardless of etiology.
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