The specificity of thalamic alterations in Korsakoff’s syndrome: Implications for the study of amnesia
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Retrograde amnesia
Retrograde amnesia is the inability to recall events which occurred immediately before head trauma or other acute brain insult. It is one aspect of a larger entity — posttraumatic amnesia — seen in some head injuries, and represents a defect in the consolidation of memories. Previous studies of retrograde amnesia have produced conflicting findings regarding its characteristics. A study was undertaken to identify the characteristics of retrograde amnesia, its relationship to anterograde amnesia, and the problems of its measurement. Forty-eight patients with head injuries admitted to the Emergency Department of the Winnipeg General Hospital were interviewed to identify all subjects meeting certain criteria regarding age, education, and so on, and twenty-five met the criteria and were included in the sample. Each subject was interviewed at least twice until the retrograde amnesia had reached a stable minimum. The duration of retrograde and anterograde amnesia as well as immediate and short-term memory were assessed. It was found that the duration of retrograde amnesia was directly related to the duration of the anterograde amnesia and to the duration of hospitalization. Some problems involved in measurement are discussed.
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Retrograde amnesia
Anisomycin
Anterograde amnesia
Memory disorder
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Retrograde amnesia
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Retrograde amnesia
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This paper reports a reassessment of published literature on the question of whether retrograde amnesia data from patients with severe trauma supports the idea that there is ongoing consolidation of long-lasting memories. That is, memory consolidation continues for decades with older memories being increasingly consolidated, and, thus, more protected from forgetting. Our analysis was limited to patients with specific traumas rather than neurodegenerative conditions that can be complicated by the additional presence of significant anterograde amnesia. These constraints were used because trauma patients have a definitive start to their amnesia allowing comparison of their memories before this event, unlike when there is an undefined amnesia onset. Our results revealed that the standard account of retrograde amnesia only fits part of the data, with more than half not conforming to this account. Specifically, damage to different brain areas was associated with different patterns of retrograde amnesia. Those cases where the standard retrograde amnesia account was held tended to involve damage to the hippocampus and temporal lobes, as expected. Future directions to better understand the influence of retrograde amnesia and memory consolidation are suggested.
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Learning and memory are important brain functions.Amnesia means loss of memory,which is divided into anterograde and retrograde amnesia.Intravenous administration of propofol or midazolam often induces retrograde amnesia in anesthetized patients, as well as with changes in dopaminergie and serotonergic activities.Changes in amount of monoamines have been proved to relate with retrograde amnesia,which may be the mechanism of propofol and midazolam anesthesia-induced retrograde amnesia.This article will review the relationship between intravenous anesthetics,monoamines and retrograde amnesia
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The permanence of retrograde amnesia produced for a single training trial by a single electroconvulsive shock was studied. No recovery from amnesia was found with either single or repeated retention tests. Amnesic effects were found to be permanent with retention intervals as long as 1 month.
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The phenomenon of retrograde amnesia has important implications for understanding normal memory as well as its neural organization. Using 6 tests of remote memory, we evaluated the extent and severity of retrograde amnesia in 2 groups of amnesic patients--7 patients with alcoholic Korsakoff's syndrome and 5 other patients with amnesia (anoxia or ischemia, N = 3; thalamic infarction, N = 1; unknown etiology, N = 1). Although there were individual differences, Experiment 1 showed that the severity and extent of retrograde amnesia was similar for the 2 groups. Retrograde amnesia was temporally graded across a period of about 15 years and was not detectable in more remote time periods. In Experiment 2, repeated testing during a 3 year period showed that amnesic patients and control subjects were similarly consistent in their responses. Amnesic patients did not catch up to control subjects by eventually accumulating as many correct answers as the control subjects. In Experiment 3, amnesic patients performed normally on a test of very difficult general information questions, which were based on material likely to have been learned long ago. In all 3 experiments, the 2 groups of amnesic patients performed similarly. The results support the following conclusions: (1) Extensive, temporally graded retrograde amnesia, which has been observed frequently in patients with Korsakoff's syndrome, occurs readily in other amnesic patients as well, even when their memory impairment appears well circumscribed; (2) patients with presumed damage to either the medial temporal or the diencephalic brain structures linked to memory functions can produce a similar kind of retrograde amnesia; (3) the impairment reflects a loss of usable knowledge, not simply difficulty accessing an intact memory store that can then be overcome given sufficient retrieval opportunities; (4) very remote memory, at least for factual information, can be intact in amnesia; (5) the structures damaged in amnesia support memory storage, retrieval, or both during a lengthy period of reorganization, after which representations in memory can become independent of these structures.
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Injections of potassium chloride into the hippocampus after learning produce temporary disruption of neural activity and retrograde amnesia. Recovery from the amnesia is selective—rats recover from amnesia of events that occurred 24 hours before injection but do not recover from amnesia of events that occurred 10 seconds before injection.
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Cortical Spreading Depression
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The amnesic and convulsive effects of experimental cerebral concussion were observed in rats. Marked convulsions were associated with only partial retrograde amnesia in one trial passive avoidance when the head injury was given less than 7 seconds after learning the task. These results are compared with the complete retrograde amnesia associated with a lesser severity of convulsions produced by electroconvulsive shock in rats under identical learning situations.
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