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Query: UMLS:C0002622 (amnesia)
5,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Becker (1988) has argued that Alzheimer's disease is particularly characterised by a combination of amnesic and dysexecutive deficits. He has supported this hypothesis by identifying patients who represent a relatively pure example of each of these. We describe a search for similarly pure patients in a sample of 55 carefully selected Alzheimer cases. We succeed in identifying one case each of relatively pure amnesia and relatively pure dysexecutive syndrome. We also, however, find cases of predominant STM deficit, as well as cases with defective visual but not verbal memory, and cases of the converse pattern. These cases do not seem to reflect simple random variation in the data, since less theoretically coherent patterns of symptoms are not found in this pure form. We conclude that AD can give rise to relatively specific cognitive deficits during its early stages, but that these do not necessarily argue for Becker's two-component interpretation of the cognitive deficit in Alzheimer's disease.
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PMID:The two-component hypothesis of memory deficit in Alzheimer's disease. 186 22

Immediate post-training intracerebroventricular administration of a synthetic peptide homologous to beta protein of brain amyloid, [Gln11]beta-(1-28), caused amnesia for footshock active avoidance training in mice in a dose-dependent fashion. This effect was specific to memory processing since the peptide did not cause amnesia when injected 24 hr after training nor did it disturb storage or retrieval of older memories. Shorter fragments of the amyloid beta protein consisting of residues 12-28, 18-28, and 12-20 also were amnestic when given intracerebroventricularly, residues 12-20 being least effective. The hippocampus, a brain structure importantly involved in learning and memory, consistently shows severe pathological changes and deposition of amyloid in patients with Alzheimer disease. Immediate post-training bilateral intrahippocampal injection of [Gln11]beta-(1-28) produced amnesia at much lower doses than did [Gln11]beta-(1-28) injected intracerebroventricularly. Thus these experimental results suggest a possible direct role of amyloid beta protein or fragments thereof in an aspect of the spectrum of cognitive deficit in Alzheimer disease.
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PMID:Amnestic effects in mice of four synthetic peptides homologous to amyloid beta protein from patients with Alzheimer disease. 201 56

We studied the parameters of suggested posthypnotic amnesia (initial deficit in recall, reversibility, and temporal disorganization of the initial material partially recalled during amnesia) in 132 psychiatric inpatients with DSM-III diagnoses of schizophrenia (N = 25), eating disorders (N = 77), alcoholism (N = 12), and major affective disorder (depression) (N = 18). We compared the findings on these patients with normal student control groups on the Stanford Hypnotic Susceptibility Scale (SHSS:C) posthypnotic suggestion item. In general, the small patient subgroups showed posthypnotic amnesia on each of these criteria in similar fashion to normal student populations. Highly hypnotizable patients were more likely to recall their hypnotic experiences in a more random order than the temporally more accurate sequence shown by low-hypnotizable subjects. Schizophrenic patients initially recalled fewer of their hypnotic experiences (indicating some cognitive deficit), and eating disorder patients initially recalled more of their experiences than other patient groups or normal subjects. Nevertheless, all patient subgroups showed significant additional recall after the reversibility cue. The results support the robustness of posthypnotic amnesia in psychiatric patients.
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PMID:Suggested posthypnotic amnesia in four diagnostic groups of hospitalized psychiatric patients. 277 18

The neurology of memory has been illuminated by parallel studies of patients with circumscribed memory impairment and animal models of human amnesia. Human amnesia can occur as an isolated cognitive deficit that impairs the ability to learn new facts and episodes. In addition, memory can be affected for material learned many years prior to the onset of amnesia. The finding that some memory abilities are intact in amnesia (e.g., skill learning, word priming, and adaptation-level effects) has suggested that memory can be divided into two or more separate processes. Declarative memory affords the ability to store information explicitly and to retrieve it later as a conscious recollection. This form of memory depends on the integrity of the structures damaged in amnesia. Other, non-declarative kinds of memory afford the ability to change as the result of experience, but the information is available only through performance. Recent studies of a favorable human case provided strong evidence that the hippocampus is a critical component of the declarative memory system. Extensive convergent and divergent projections link the hippocampus to many areas of neocortex where processing and storage of new information is likely to occur. It is perhaps by way of these connections that the hippocampus operates upon and participates in declarative representations.
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PMID:The organization and neural substrates of human memory. 298 Jun 90

Recent studies have indicated that impairment of memory is a common cognitive deficit related to long-term alcohol consumption. Such deficits range from subtle disturbance through a "subclinical" amnesic disorder to full-blown Korsakoff syndrome. This finding is congenial with the hypothesized continuum of alcohol-related impairment of memory. Among alcoholics, this memory impairment appears to be etiologically distinct from the commonly observed deficits in abstracting and problem-solving abilities. In the present chapter, a dual and a unitary formulation of memory are contrasted in their ability to present a coherent account of what memory tasks Korsakoff amnesics can and cannot do. The explanations offered by unitary theory are weak compared to those derived from the theory that memory consists of two distinct systems--experiential and abstractive memory. We indicate how the pattern of responding on standard clinical tests of memory can be coherently analyzed post hoc within the dual formulation. A number of experimental predictions are also presented based on the theory that Korsakoff amnesics have a profound impairment of experiential memory, whereas the abstractive system is essentially normal. Such experiments should clarify the nature both of Korsakoff amnesia and of memory itself. In conclusion, we indicated that memory disorders related to alcoholism can be understood in terms of a gradient, or continuum, of impairment of the experiential system.
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PMID:The chronic effects of alcohol on memory. A contrast between a unitary and dual system approach. 355 Sep 17

A 2 1/4-year prospective study of children suffering head injury is described. Three groups of children were studied: (a) 31 children with 'severe' head injuries resulting in a post-traumatic amnesia (PTA) of at least 7 days; (b) an individually matched control group of 28 children with hospital treated orthopaedic injuries; and (c) 29 children with 'mild' head injuries resulting in a PTA exceeding 1 hour but less than 1 week. Individual psychological testing was carried out as soon as the child recovered from PTA, and then again 4 months, 1 year, and 2 1/4 years after the injury. A shortened version of the Wechsler Intelligence Scale for Children (WISC), the Neale Analysis of Reading Ability and a battery of tests of specific cognitive functions were employed. The mild head injury group had a mean level of cognitive functioning below the control group, but the lack of any recovery; during the follow-up period indicated that the intellectual impairment was not a consequence of the injury. In the severe head injury group, the presence of cognitive recovery and a 'dose-response' relationship with the degree of brain injury showed that the intellectual deficits were caused by brain damage. Some degree of cognitive impairment was common following head injuries giving rise to a PTA of at least 2 weeks. Conversely no cognitive sequelae, transient or persistent, could be detected when the PTA was less than 24 hours. The results were less consistent in the 1-day to 2-week PTA range, but the evidence suggested that a broadly defined threshold for impairment operated at about that level of severity of injury. Timed measures of visuo-spatial and visuo-motor skills tended to show more impairment than verbal skills but otherwise there was no suggestion of a specific pattern of cognitive deficit. Recovery was most rapid in the early months after injury, but substantial recovery continued for 1 year with some improvement continuing n the second year in some children, especially those with the most severe injuries. Age, sex and social class showed no significant effects on the course of recovery.
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PMID:A prospective study of children with head injuries: II. Cognitive sequelae. 720 46

Electroconvulsive therapy (ECT) is a safe, effective, valuable treatment for serious affective disorders (eg, major depression). Sometimes indicated for other, occasionally nonpsychiatric, medical conditions, ECT is a moderately complex procedure for which training is provided routinely during psychiatric residency. Although temporary confusion and amnesia are expected immediately after treatment, no reliable data suggest that permanent memory loss or cognitive deficit is caused by modern ECT. Indeed, because severe depression itself often causes both memory and cognitive deficits, ECT's remarkable therapeutic effectiveness is associated with long-term improvement in cognition, learning ability, and memory for many patients. Controversy over safety and effect on memory is fueled largely by public misinformation.
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PMID:Electroconvulsive therapy. 834 62

The behavioral activity of the thyrotropin-releasing hormone (TRH) analogue, L-6-ketopiperidine-2-carbonyl-leucyl-L-prolinamide (RGH 2202), has been studied in animal models of central neurotransmission disruption. In 24-month-old rats, repeated administration of the peptide (5 or 10 mg/kg/day, injected IP for 20 days) was followed by a facilitated acquisition of active avoidance behavior in the shuttle-box test and retention of passive avoidance reaction in a step-through passive avoidance task. Also, ambulation in an open field was increased and motor performance and co-ordination in the rotorod test was facilitated by the treatment. Scopolamine-induced amnesia was reverted by RGH 2202 in adult rats tested both in active and passive avoidance tasks. Cognitive deficits induced in rats by prenatal manipulation with methylazoxymethanol (MAM) were reduced in adulthood by repeated administration with RGH 2202. These results indicate that the TRH-analogue, RGH 2202 may improve cognitive and motor disturbances in aging or induced by central neurotransmission disruption. It is possible that the peptide is functioning, at least in part, by intervening with the central cholinergic neurotransmission.
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PMID:Effects of RGH 2202 on cognitive and motor behavior of the rat. 878 5

The aim of this study was to reevaluate short term and long term memory disorders after anterior communicating artery rupture, then to more specifically assess the importance and the role of forgetting, proactive and retroactive interferences, impaired memory for temporal order, attention disorders and dysexecutive syndrome, and finally MRI-defined brain lesions. Twenty one patients presenting with selective anterior brain injury, were assessed at the secondary and late post stroke phases. The short term memory analysis showed the digit span was reduced at the secondary stage, but that mean performances were preserved in the Peterson and Sternberg paradigms. Verbal and visuospatial learning in long term memory showed a severe deficit in free recall, chiefly serial, and associative recall. Recognition was mildly impaired at the secondary phase, and later normalized. A definite and lasting increase of proactive and retroactive interferences and an impairment in discriminating the temporal order of word presentations were observed. Amnesic impairment was relatively well correlated with forgetting, severity of interferences and temporal order amnesia, so as with disorders of attention and executive functions (Wisconsin Card Sorting Test). However, intrusions in free recall and false recognitions were not clearly related with the dysexecutive syndrome. The severity of amnesia was associated with lesions of the left anterior cingulate cortex, and of the corpus callosum. These results suggest that these patients mainly had a deficit in information retrieval, mostly compromising long term memory, but also to a lesser degree short term memory. Forgetting, interferences and the dysexecutive syndrome probably play an important role in the decline of mnemonic performance, but do not clearly explain intrusions in recall and errors in recognition.
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PMID:[Learning disorders after ruptured aneurysms of the anterior communicating artery]. 977 84

The development of cholinergic therapies for Alzheimer's disease (AD) has highlighted the importance of understanding the role of attentional deficits and the relationship between attention and memory in the earliest stages of the disease. Variability in the tasks used to examine aspects of attention, and in the disease severity, between studies makes it difficult to determine which aspects of attention are affected earliest in AD, and how attentional impairment is related to other cognitive modules. We tested 27 patients in the early stages of the disease on the basis of the MMSE (minimal 24-30 corresponding to minimal cognitive impairment, very mild or possible AD in other classifications; and mild 18-23) on a battery of attentional tests aimed to assess sustained, divided, and selective attention, plus tests of episodic memory, semantic memory, visuoperceptual and visuospatial function, and verbal short-term memory. Although the mildly demented group were impaired on all attentional tests, the minimally impaired group showed a preserved ability to sustain attention, and to divide attention based on a dual-task paradigm. The minimally demented group had particular problems with response inhibition and speed of attentional switching. Examination of the relationship between attention and other cognitive domains showed impaired episodic memory in all patients. Deficits in attention were more prevalent than deficits in semantic memory suggesting that they occur at an earlier stage and the two were partially independent. Impairment in visuoperceptual and visuospatial functions and verbal short-term memory were the least common. Although attention is impaired early in AD, 40% of our patients showed deficits in episodic memory alone, confirming that amnesia may be the only cognitive deficit in the earliest stages of sporadic AD.
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PMID:The nature and staging of attention dysfunction in early (minimal and mild) Alzheimer's disease: relationship to episodic and semantic memory impairment. 1067 92


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