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

Speed of forgetting by the patient H.M. was examined in two experiments using picture recognition tests. In both experiments stimulus duration was manipulated to equalize initial performance by H.M. and others, and speed of forgetting was investigated over a period of one week. In the first experiment, where initial performance was high, H,M. appeared to forget faster than normal controls. In the second experiment, where initial performance was somewhat lower, H.M. was shown to forget faster than both controls and Korsakoff patients (who forget at a normal rate). These results suggest a functional difference between the amnesia with hippocampal lesions and the amnesia of Korsakoff's disease.
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PMID:Normal and abnormal forgetting in organic amnesia: effect of locus of lesion. 54 May 10

This study investigated the intercorrelation of 8 'frontal' tests in 32 patients with Korsakoff's syndrome and Alzheimer's disease, and examined the relationship of frontal dysfunction to impaired release from proactive interference and impoverished retrieval from retrograde memory. Amongst the frontal tests, there were statistically significant intercorrelations between 3 'fluency' tests and 3 'card-sorting' tests, although the degree of shared variance was relatively low. The relationship of another test--picture arrangement errors--was more equivocal; performance for 'cognitive estimates' was unrelated to performance in the other frontal tests, possibly because it may reflect pathology at a different frontal site. There was no evidence in this study that variability in release from proactive interference was related to measures of frontal function in either patient group, and the conditions under which these patient groups fail to show 'normal' release appear to be tightly constrained. On the other hand, the defective retrieval of retrograde memories was correlated with frontal dysfunction in both patient groups. There was a suggestion of a double dissociation with a measure of nonverbal short-term forgetting, impairment at which was related to the degree of general cortical atrophy rather than frontal dysfunction. A stepwise regression equation based on 3 frontal tests could account for 64% of the variability in retrograde memory performance within the total patient group, 68.5% in the Korsakoff group and 57% in the Alzheimer group. By comparison, the severity of anterograde memory impairment predicted only 21% of the variance in retrograde memory performance. It is concluded that frontal dysfunction produces a disorganization of retrieval processes which contributes to the temporally-extensive retrograde amnesia of these two disorders.
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PMID:Frontal dysfunction and memory deficits in the alcoholic Korsakoff syndrome and Alzheimer-type dementia. 199 78

After initial learning had been equated as closely as possible, 16 Alzheimer-type dementing patients showed the same rate of forgetting on a picture recognition test administered at intervals over the course of a week as 16 Korsakoff patients and 16 healthy controls. This suggested that the anterograde amnesic deficit in both Alzheimer's disease and Korsakoff's syndrome is primarily an acquisition or learning deficit. The Alzheimer patients differed from both the Korsakoff patients and the healthy controls in showing diminished digit span and severely impaired performance at the Brown-Peterson test, implicating a deficit of short-term (or working) memory. The variability of performance within groups on the principal tests employed was also examined; and the Alzheimer results are discussed with respect to the underlying neuropathology, and the implication for pharmacotherapy.
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PMID:Rates of forgetting in Alzheimer-type dementia and Korsakoff's syndrome. 405 8

An analysis of forgetting was applied to patients with Korsakoff's syndrome, patients receiving bilateral electroconvulsive therapy (ECT), and case N. A. who has chronic amnesia for verbal material. Patients with Korsakoff's syndrome and case N. A. exhibited a normal forgetting rate, whereas patients receiving ECT exhibited abnormally rapid forgetting. Based on previous findings for the patient H. M., on indirect evidence that the amnesia associated with ECT might be related to temporal lobe dysfunction, and on the diencephalic distribution of lesions in case N. A. and in Korsakoff's syndrome, these results support the hypothesis that these amnesias are distinct syndromes of memory dysfunction. Thus, the stage of memory function disrupted may be different in the two circumstances, and medial temporal and diencephalic brain regions may normally contribute in different ways to the formation of memory.
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PMID:Two forms of human amnesia: an analysis of forgetting. 734 71

This study further examines the performance of diencephalic and temporal lobe amnesics on the recency judgement task (Parkin, Leng and Hunkin, 1990). The two patient groups were represented by patients with Wernicke-Korsakoff syndrome (WKS) and post-Herpes simplex encephalitis (HSE). Experiment 1 demonstrated that poorer recency judgements by WKS patients were not due to a general proactive interference effect, but from an inability to remember which items had been designated targets on a given trial. Experiment 2 demonstrated that the superior performance of the HSE group was not attributable to a putative faster forgetting rate. In addition, the study found no relationship between recency judgements and degree of frontal lobe impairment. It is concluded that diencephalic damage has a particular effect on the ability to make recency judgements and that this represents a fundamental difference between diencephalic and temporal lobe amnesia. Theoretical interpretations of this difference are discussed.
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PMID:Recency judgements in Wernicke-Korsakoff and post-encephalitic amnesia: influences of proactive interference and retention interval. 825 87

We tested amnesic and control subjects on a task which required the recognition of single, difficult to name colours, after delays ranging from 7 seconds to 120 seconds after performance of the two subject groups had been matched at the shortest delay by giving the amnesic patients longer study time. The amnesic patients showed abnormally fast forgetting over the two minute period. Furthermore, a subgroup of nine subjects with presumed damage to midline diencephalic structures (Korsakoff's syndrome) were found to forget as fast as a group of six subjects with presumed medial temporal lobe damage (herpes simplex encephalitis). These results contrast both with studies using the Huppert and Piercy procedure and those using the Brown-Peterson task, none of which have shown convincing evidence of accelerated forgetting in medial temporal lobe or diencephalic amnesia.
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PMID:Do amnesics forget colours pathologically fast? 966 1

Memory and forgetfulness have been viewed since antiquity from perspectives of physical, emotional, and spiritual states of well-being, and conceptualized philosophically. Numerous discussions of memory loss, or case reports, existed, but a fundamental advance in conceptualization of memory loss as a pathological clinical phenomenon originated when Sauvages classified "amnesia" as a medical disorder, in 1763. Originally, amnesia was recognized as a weakening or dissolution of memory, according to a taxonomy that ascribed known causes to the disorder. Etiologic factors included neurological disorders of stroke, hemorrhage, and head injury, metabolic dysregulation, alcohol and substance abuse, toxicity, anoxia, and other acute or chronic (sometimes progressive) brain disorders. Clinical descriptions of amnesia appeared internationally in medical dictionaries and scientific encyclopedias in the early 19th century. The possibility that amnesia could be either idiopathic, or symptomatic of another illness, was proposed based on the wide range of recognized etiologies and associations. Debate ensued regarding the status of amnesia as an illness or a symptom, but regardless, amnesia was soon recognized as an independent disorder of memory, distinguishable from disorders of global intellect, or of consciousness, or of language. Distinctions of amnesia considered its temporal gradient, duration and natural course, nature of onset, severity or depth of memory loss, course, and prognosis. Concepts of retrograde (forgetting knowledge preceding onset) and anterograde (difficulty learning, recalling new information) further specified the nature of amnestic memory difficulty. Alcoholic amnesia in Korsakoff's syndrome generated much attention. Amnesia as a clinical feature was critical to the development of notions of dissociation of conscious from subconscious recall in hysteria, and differentiation of neurogenically-based from psychogenically-based amnesia became central to understanding post-traumatic states. Amnesia studied as a disorder of memory remains an avenue to enrich clinical understanding of a condition that continues to be powerfully challenging to this day.
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PMID:Early History of Amnesia. 3122 Aug 49