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Query: UMLS:C0598853 (forgetting)
 3,232 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This article presents first a short historical overview of the different viewpoints concerning psychiatric approaches to define the concept "amnesia" (Ribot, Korsakow, K. Schneider, Bleuler, Bonhoeffer et al.). A generally accepted result is the differentiation between retrograde and anterograde amnesia. Research work of the last two decades has focussed on the experimental investigation of anterograde amnesia, the so-called amnesic syndrome. In this context four main factors responsible for memory performance are distinguished: encoding, retrieval, forgetting and interference. One of the main results of neuropsychological research in amnesia consists in having discovered a set of symptoms or features common to most if not all forms of amnesia. These features appear regardless of etiology and locus of lesion. This set or features is described in detail in the paper. On the basis of these amnesic features a clinical test was developed, the Berliner Amnesie Test (BAT). This standardized test can be used for the assessment from mild up to severe memory disorders.
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PMID:[The concept of amnesia and quantitative assessment of amnesic disorders]. 188 18

The present research was concerned with anterograde and retrograde memory for a socially transmitted food preference in rats with lesions to the dorsal hippocampus or dorsomedial thalamus, and operated controls. In Expt. 1, food-preference training was administered postoperatively and memory was tested following various delays. Both lesioned groups acquired the preference normally, but rats with hippocampal lesions displayed a rapid rate of forgetting that indicated significant anterograde amnesia. In Expt. 2, the food preference was acquired at different times preoperatively and retrograde memory was tested postoperatively. Both lesioned groups exhibited loss of memory when training immediately preceded surgery, but only rats with hippocampal lesions displayed a temporally-graded retrograde amnesia. The results confirmed the differential effects of hippocampal and thalamic lesions on memory performance. It was suggested that memory loss following thalamic lesions was related to factors associated with original learning, whereas the pattern of hippocampal amnesia reflected disruption at a later stage in the learning process.
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PMID:Anterograde and retrograde amnesia in rats with dorsal hippocampal or dorsomedial thalamic lesions. 236 34

In animals, as in humans, benzodiazepines affect memory, inducing almost exclusively an anterograde amnesia. The characteristics of this amnesic-like effect are reviewed in terms of alterations in acquisition, consolidation, recall and/or forgetting processes. Explanations alternative to a true amnesia, i.e., state-dependent learning, cognitive deficits, attenuation of the emotional weight of the conditioning events are examined. Finally, the interference of these putative amnesic effects with experimental procedures devoted to the study of the anxiolytic activities of benzodiazepines are considered.
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PMID:Some evidence for amnesic-like effects of benzodiazepines in animals. 285 85

The effect of cholinergic 'blockade' on human memory performance as a model for the effect of cholinergic depletion in clinical disorders was investigated. A wide range of memory functions was assessed in 70 subjects, using tests which were identical or closely similar to those which have previously been employed in clinical studies of Alzheimer and Korsakoff patients. In addition, a physiological measure of the degree of central cholinergic blockade was included, as well as measures of subjective arousal and objective attention. It was found that cholinergic blockade had no significant effect on the more passive aspects of primary (or 'working') memory, namely span tests and a measure of verbal short-term forgetting; in this, it contrasts with the marked deficits seen in Alzheimer-type dementia. On the other hand, cholinergic blockade produced impairment at a visuospatial short-term forgetting test, and at a verbal test in which the distractor task was made more difficult. On tests of secondary memory, cholinergic blockade produced a pattern similar to that seen in the anterograde amnesia of Alzheimer and Korsakoff patients, namely a pronounced impairment in learning verbal and visuospatial material, a 'normal' forgetting rate once learning had been accomplished, and relative preservation of the response to priming and of skill learning (procedural memory). Cholinergic blockade, however, did not produce a retrograde amnesia, nor did it affect the recall of temporal context or of long-established semantic knowledge. This pattern of results is compared with that obtained in previous studies of Alzheimer and Korsakoff patients.
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PMID:Cholinergic 'blockade' as a model for cholinergic depletion. A comparison of the memory deficits with those of Alzheimer-type dementia and the alcoholic Korsakoff syndrome. 317 85

This paper describes the clinical features of selected examples of organic and psychogenic amnesia, and it discusses the nature of the dysfunction that these amnesias entail. The anterograde component of organic amnesia involves a severe impairment in acquiring (or learning) new information, rather than accelerated forgetting, and this may reflect an underlying limbic or neurochemical dysfunction. Retrograde amnesia has a basis which is (at least partially) independent of anterograde amnesia--in some patients, it appears to involve a failure to reconstruct past experience from contextual cues, and this may reflect a super-imposed frontal dysfunction. Two types of confabulation are discussed, one of which ('provoked') is a normal response to poor memory, and the other ('spontaneous') appears to reflect incoherent, context-free retrieval, associated with more severe frontal pathology. It is argued that many cases of psychogenic amnesia may resemble organic amnesia, in that they result from an impaired acquisition of information at the time of initial input, perhaps thereby predisposing the subject to subsequent retrieval difficulties.
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PMID:Amnesia: organic and psychogenic. 331 Dec 68

Anterograde amnesia (AA), forgetting of events that occur following a traumatic episode, has recently been demonstrated by using a mild decrease in temperature (hypothermia) as the amnestic agent. However, no data currently exist to indicate if an increase in body temperature (hyperthermia) might affect memory processing in a similar manner. Experiments 1 and 2 demonstrated that increasing the colonic body temperature of the rat to 3-4 degrees C or more above normal during avoidance training produced a significant retention loss when the test occurred 24 hr after training. Slight hyperthermia to 1-2 degrees C above normal did not impair retention. In Experiment 3, AA resulting from an elevation in temperature was reversed by reheating "amnestic" subjects just prior to the 24-hr test. By rapidly reversing hyperthermia immediately after the training trial with a cooling procedure, Experiment 4 demonstrated that hyperthermia-induced AA was not the result of retrograde influences of the heating treatment. Implications of these results are discussed in terms of possible retention deficits which could conceivably follow environmental heat stress or fever hyperthermia resulting from bacterial infection.
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PMID:Anterograde amnesia induced by hyperthermia in rats. 349

The present investigation examined whether the poor test performance observed in studies of anterograde amnesia reflects a memory deficit or is a by-product of weaker initial learning resulting from impaired sensory, motivational, or associative processes. Two experiments were performed which utilized latent extinction (Experiment 1) and delay of punishment (Experiment 2) manipulations in order to assess the nature of original learning in rats trained under either hypothermic (29 degrees C) or normothermic conditions. Results from both experiments provided evidence that hypothermia treatment administered prior to training had relatively little influence on the animal's ability to acquire a passive avoidance response. Therefore, the rapid forgetting observed in hypothermia-induced anterograde amnesia is most likely due to memory deficits rather than an artifact of poorer acquisition.
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PMID:Hypothermia-induced anterograde amnesia: is memory loss attributable to impaired acquisition? 363 48

The effect of hippocampal denervation on olfactory memory in rats was tested after interrupting the lateral olfactory tract projections at the level of the entorhinal cortex. When lesioned animals were trained to learn new odors, they showed no evidence of retention 3 h after acquisition. These results confirm earlier data on rapid forgetting in rats after hippocampal deafferentation and are in parallel to the anterograde amnesia typically found in humans with hippocampal damage. On the other hand, preoperatively learned information was minimally impaired after hippocampal deafferentation even if it was acquired within less than 1 h before the lesion. This finding differs from reports on humans as well as monkeys with hippocampal damage where memories formed during a critical time span of months or even years before the lesion are found to be impaired. This may suggest that the consolidation process in humans and rodents has different time scales or that the roles of the human and the rat hippocampal structure in memory formation are somewhat different.
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PMID:Studies on retrograde and anterograde amnesia of olfactory memory after denervation of the hippocampus by entorhinal cortex lesions. 381 47

To analyse the neural basis of long-term memory, recordings were made from single neurons in monkeys performing a visual recognition task of the type impaired in anterograde amnesia in man. Each visual stimulus was shown twice per day, once as novel, and after 0 to 17 other intervening items in the recognition task, on a second trial, as familiar, when the monkey could lick to obtain fruit juice if he recognized the stimulus correctly. At the anterior border of the thalamus, a population of neurons was found which responded to the stimuli only when they were familiar. The activity of these neurons was not related to lick responses. Further, in a different, visual discrimination, task, a number of these neurons were found to respond both to the familiar rewarded stimulus to which the monkey always licked, and to the familiar aversive stimulus to which he did not lick. This shows that in a reward association task these neurons respond on the basis of familiarity, providing evidence for a dissociation of recognition and associative memories. Analysis of the responses of these neurons in the continuous visual recognition task showed that the responses to familiar stimuli were time-locked to the onset and duration of the visual stimulation (brief exposures producing brief responses). The response latencies were in the range 100 to 200 ms. A 100 ms exposure of the stimulus was sufficient for the stimulus to be encoded, and a 100 ms exposure was also sufficient for a recognition related response. The magnitude of the neuronal response on trials with familiar stimuli decreased as the number of trials between the first (novel) and second (familiar) presentation of the same stimulus increased. The rate of this decay or 'forgetting' varied from cell to cell and was best described by an exponential function. Repeated exposure tended to slow the rate of forgetting, and two or three repeated presentations prolonged some cell 'memories' for more than 100 intervening trials. Although the majority of the neurons did not have such long 'memories', in that they responded as novel to stimuli seen on a preceding day, so that their responses could be related to recency but not to absolute recognition of ever having seen a stimulus before, 2 neurons did respond to stimuli which had not been seen for 24 h. The neurons showed some ability to respond to stimuli as familiar despite changes in viewing conditions and transformations such as 90 deg rotation. These findings indicate that the responses of these neurons at the anterior border of the thalamus are activated during recency or longer term recognition processing, both of which are impaired in anterograde amnesia in man. Measurement of the responses of these neurons, which appear to have access to memory mechanisms, has allowed parameters affecting such memory mechanisms to be investigated.
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PMID:Neuronal responses related to visual recognition. 689 Mar 95

The present study was aimed at determining whether or not lesions of the anterior thalamic nuclei induced deficits in sequential or delayed spatial alternation (SA) in mice, these procedures enabling measures of sensitivity to interference and rate of forgetting respectively. Results showed that sequential SA comprising six successive trials separated by a 30 s inter-trial interval was not impaired by the lesion; in contrast, delayed SA in lesioned animals was impaired by a long (6 h) but not by a short (5 min) delay, compared with controls. These results support the view that lesions of anterior thalamic nuclei can produce anterograde amnesia for spatial informations selective to relatively long delay.
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PMID:Effects of anterior thalamic lesions on spatial memory in mice. 806 Dec 96


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