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Query: UMLS:C0751295 (memory loss)
 3,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A word recognition task was designed to determine the stage in memory affected by a single 10-mg intravenous injection of diazepam and the duration of the effect. Injection in three experimental subjects produced an anterograde amnesia for the 14 to 24-minute period immediately after injection. Memory loss resulted from impaired storage, the stage during which information is entered into memory. Retention and retrieval stages of memory were unaffected. This temporary amnesia may result from increased inhibition in the hippocampal system produced by diazepam, which shares many properties with the inhibitory neurotransmitter gamma-aminobutyric acid.
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PMID:The pattern of memory loss resulting from intravenously administered diazepam. 44 98

Benzodiazepines, shown to affect memory, can produce anterograde amnesia (i.e., a loss of memory for events occurring forward in time). Following the ingestion of a benzodiazepine, short-term memory is not affected, but long-term memory is impaired. The memory loss may occur because events are not transferred from short-term memory to long-term memory and thus not consolidated into memory storage. Information stored prior to the ingestion of a benzodiazepine is not affected. Memory impairment is more likely in benzodiazepines that have a high benzodiazepine-receptor affinity, that accumulate in the body, that are given in high doses or intravenously, or that are eliminated slowly. Individuals taking benzodiazepines are often unaware of their memory impairment unless it is pointed out to them. Elderly clients experiencing memory impairment may be embarrassed to mention the problem. Alternatives to prescribing benzodiazepines include antidepressant medications, exercise or psychotherapy. When prescribing a benzodiazepine, it is important to fully inform patients of the drug's potential side effects and to maintain the lowest effective dose for the shortest period of time.
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PMID:Anterograde amnesia linked to benzodiazepines. 809 35

Effects of exposure to halothane on memory processing was studied using single-trial inhibitory avoidance learning to measure retention. Mice were anesthetized with halothane either before training, immediately after training, or both before training and before testing. Results showed that memory was not impaired by posttraining halothane exposure, indicating that the anesthetic does not cause retrograde amnesia. Mice trained after recovery from halothane showed a robust memory loss 24 h later. This deficit could be alleviated by reexposure to the anesthetic before the retention test. Mice given multiple training trials following recovery from the anesthetic showed a normal rate of learning when compared with controls, but deficient retention. This indicates that the performance deficit was the result of impaired retention (anterograde amnesia) rather than disrupted acquisition. Anterograde amnesia occurred when training was delayed up to 2 h after recovery from anesthesia. These findings indicate that the memory impairment following halothane anesthesia is the result of a state-dependent retrieval failure.
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PMID:Halothane anesthesia causes state-dependent retrieval failure in mice. 140 4

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

Anterograde amnesia refers to the inability to form new memories. Alcoholic blackout, benzodiazepine-induced amnesia and transient global amnesia are three disorders that result in acute transient memory loss. These disorders may be difficult to recognize, because the memory loss is not usually accompanied by other symptoms of neurologic impairment.
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PMID:Acute transient memory loss. 280 70

To investigate experimentally the mnemonic and neuropathological effects of blockage of the posterior cerebral arteries (PCA), a cerebrovascular accident that can lead to global anterograde amnesia in humans, we permanently occluded these arteries bilaterally in six monkeys and then evaluated their performance on a visual recognition task, after which we assessed the extent of their ischemic infarcts. The latter showed substantial individual variation, ranging from almost no damage in one case to massive unilateral injury of both the ventromedial o occipitotemporal cortex and hippocampal formation in another. In the four remaining cases, however, the infarcts fell within a narrow range, being confined almost entirely to the hippocampal formation and parahippocampal gyrus, and then only to restricted portions of these structures, unilaterally in one case, and bilaterally in the three others. Performance on the recognition task was related to the presence and bilaterality of the hippocampal injury. Thus, the case without any hippocampal damage performed at a rate equal to that of normal controls; the case with unilateral hippocampal damage was mildly impaired; and the three cases with bilateral infarctions, involving between 20 and 55% of the hippocampal formation, showed substantial impairment, with scores averaging 20% below those of normal controls. The only subfields of the hippocampus damaged in common in these cases were CA1 and CA2. Paradoxically, the memory loss found in these three animals with only partial bilateral hippocampal damage was significantly greater than that found in animals with total bilateral ablation of the hippocampal formation, whose scores averaged only 10% below those of normal controls. Possible explanations for this extremely puzzling outcome are proposed.
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PMID:Mnemonic and neuropathological effects of occluding the posterior cerebral artery in Macaca mulatta. 271 Mar 18

In anterograde amnesia, memory loss is obtained for events that occur subsequent to the traumatic insult. But because the effects of an anterograde agent or treatment usually last for minutes, or even hours, after the nominal training event, processing of information may be altered during the postacquisition period as well as during acquisition. Since posttraining manipulations are themselves capable of modulating memory, or inducing retrograde amnesia, the memory loss due to a putative anterograde treatment may instead represent retrograde processes. The present experiment examined this potential source of confounding by using an amnestic treatment that can be quickly reversed after training in order to remove postacquisition effects. Thus, the presence of amnesia would isolate anterograde contributions as the source of loss. For induction of anterograde amnesia, rats were trained while at reduced body temperature (29 degrees C). A rapid rewarming procedure was introduced for some animals immediately after training to ensure that the hypothermic state did not extend into the postacquisition period. Other subjects were rapidly rewarmed 1 hr after training to control for any effects of the rewarming manipulation. Both groups showed severe anterograde amnesia that was indistinguishable from that obtained in the gradually rewarmed controls. These data provide an empirical example of an anterograde-induced memory deficit that is independent of retrograde influences.
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PMID:Is anterograde amnesia a special case of retrograde amnesia? 687 Oct 37

Human amnesia cases (after surgical removal of the hippocampi or brain anoxia) have clearly established the critical role of the hippocampal formation in anterograde amnesia. Other parts of the brain may also contribute to anterograde amnesia (mammillary bodies, medial thalamus). In neurodegenerative diseases (and specially in Alzheimer's disease) amnesia is often the prominent symptom, but the brain lesions are not restricted to the hippocampal formation. In Alzheimer's disease they involve also the cerebral cortex and several subcortical nuclei. Physiological brain aging is also associated with some degree of memory impairment, but much less severe than in Alzheimer's disease. The issue of the nature and the mechanisms of the memory impairment associated with age and with Alzheimer's disease is very important, because the frequency of these problems increases dramatically as the populations of the world is growing older. There is some evidence that neuronal loss and alterations in neurotransmitter systems occur in the aged subject, but the relationship between such changes and the age-related memory deficit is far from being clear. In Alzheimer's disease, the loss of memory is likely to be due to neuronal loss in cerebral cortex and hippocampal formation, along with alterations in neurotransmitter systems (specially cholinergic, monoaminergic and aminoacidergic systems). The work in experimental animals has largely confirmed the critical role of the hippocampal formation, as well as identified other critical structures. The mechanisms of the age-related memory impairment can be to some extent investigated in aged animals. In the aged rat there is evidence that several neurotransmitter networks are altered. Alteration in the dopaminergic and cholinergic systems have been extensively studied, but the involvement of other systems is likely. Learning and memory deficits are consistently observed in a sub-population of aged rodents (as well as in other species including non-human primates). For instance some aged rats do have a deficit in the performance of a spatial learning task such as the "water maze". There is some evidence that this deficit is due, at least in part, to alterations in the functions of the hippocampal formation. In other words, if aged rats have a spatial memory deficit, it might be due to changes in hippocampal neuronal circuitry. The study of age-related alterations in hippocampal neuronal networks, using electrophysiological techniques have shown that several neuronal properties such as resting membrane potential, membrane resistance or sodium spike amplitude are not altered in the aged rat hippocampus.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Aging of memory mechanisms]. 778 Jul 90

Retrograde amnesia for autobiographical material in the absence of anterograde amnesia or other memory disturbances was found in a patient with acute viral encephalitis. Memory loss showed a temporal gradient, but new learning was spared. Both brain perfusion imaging with 99mTc-HMPAO SPECT, and EEG localized the lesion in the left temporal lobe while CT and MRI were normal. This observation supports the anatomical differentiation between the different memory functions. The uncommon combination of isolated retrograde amnesia without other neuropsychological findings may raise the doubt of psychogenic aetiology, which in this case was refuted.
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PMID:Isolated retrograde amnesia for autobiographical material associated with acute left temporal lobe encephalitis. 779 57

The patient was a right-handed 59-year-old female technician who was admitted to our hospital with a complaint of memory loss. Clinical examination revealed pure anterograde amnesia regarding episodic memory, while semantic and procedural memory was intact. Radiological procedures (CT scan and MRI) revealed a tumor of the septum pellucidum, which localized from the lower part of the corpus callosum to the anterior parts of the bilateral fornices. Transcallosal total removal was performed (pathological examination revealed that it was astrocytoma). Radiological and operative findings showed that the thalamus, the mammillary bodies, the hippocampus, and the basal forebrain, which are closely related to memory, were spared. After the operation, she reported no further memory disturbance. Preoperative neuropsychological tests revealed anterograde amnesia for verbal and visual stimuli, but postoperatively the former disappeared and the latter improved. Pre- and postoperatively, she was nonaphasic, and her immediate memory, intelligence, and frontal functions were intact. Cases of amnesia due only to fornix lesions are rare, and have not been reported yet in Japan. Our case is valuable in terms of showing that only the fornix lesion was responsible for memory disturbance. The main symptom resulting from fornix lesion is thought to be anterograde amnesia.
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PMID:[Pure anterograde amnesia due to bilateral fornix lesions]. 783 48


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