Journal articles: 'Amnesia'

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Bertrand, Lorne D., and Nicholas P. Spanos. "The Organization of Recall during Hypnotic Suggestions for Complete and Selective Amnesia." Imagination, Cognition and Personality 4, no. 3 (March 1985): 249–61. http://dx.doi.org/10.2190/rfxd-0l4n-ccfe-rnge.

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Hypnotic subjects learned a nine item list that contained three words in each of three categories. Afterwards, they were instructed to forget either the entire list, the items in one category, or one item from each category. Clustering of recall was measured on the recall trials immediately before the suggestion, during amnesia testing, and after cancelling the suggestion. Partial amnesics asked to forget the entire list clustered significantly less during amnesia testing than before or after the suggestion, and testified that they shifted attention away from the recall task during amnesia testing. Subjects in the two selective amnesia treatments showed high levels of clustering during amnesia testing. Instead of disattending from the recall task at this time, these subjects devised strategies for segregating the to-be-forgotten and to-be-remembered items. These findings support the hypothesis that hypnotic amnesia involves strategic enactment, and that amnesic subjects maintain control over their memory processes.

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Daum, Irene, Herta Flor, Susann Brodbeck, and Niels Birbaumer. "Autobiographical Memory for Emotional Events in Amnesia." Behavioural Neurology 9, no. 2 (1996): 57–67. http://dx.doi.org/10.1155/1996/362301.

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This study investigated autobiographical memory for emotionally flavoured experiences in amnesia. Ten amnesic patients and 10 matched control subjects completed the Autobiographical Memory Interview and three semi-structured interviews which assessed memory for personal events associated with pain, happiness and fear. Despite retrograde amnesia for autobiographical facts and incidents, amnesics remembered a similar number of emotionally significant personal experiences as control subjects. Their recollections generally lacked elaboration and detail, but pain-related memories appeared to be more mildly impaired than memories associated with happiness and fear. The findings are discussed in relation to recent views on the relationship between affect and memory.

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Kopelman, M. D. "Amnesia." British Journal of Psychiatry 150, no. 4 (April 1987): 428–42. http://dx.doi.org/10.1192/bjp.150.4.428.

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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 superimposed 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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Kinder, Annette, and David R. Shanks. "Amnesia and the Declarative/Nondeclarative Distinction: A Recurrent Network Model of Classification, Recognition, and Repetition Priming." Journal of Cognitive Neuroscience 13, no. 5 (July 1, 2001): 648–69. http://dx.doi.org/10.1162/089892901750363217.

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A key claim of current theoretical analyses of the memory impairments associated with amnesia is that certain distinct forms of learning and memory are spared. Supporting this claim, B. J. Knowlton and L R. Squire found that amnesic patients and controls were indistinguishable in their ability to learn about and classify strings of letters generated from a finite-state grammar, but that the amnesics were impaired at recognizing the training strings. We show, first, that this pattern of results is predicted by a single-system connectionist model of artificial grammar learning (AGL) in which amnesia is simulated by a reduced learning rate. We then show in two experiments that a counterintuitive assumption of this model, that classification and recognition are functionally identical in AGL, is correct. In three further simulation studies, we demonstrate that the model also reproduces another type of dissociation, namely between recognition memory and repetition priming. We conclude that the performance of amnesic patients in memory tasks is better understood in terms of a nonselective, rather than a selective, memory deficit.

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O'CONNOR, MARGARET G., and GINETTE M. C. LAFLECHE. "Retrograde amnesia in patients with rupture and surgical repair of anterior communicating artery aneurysms." Journal of the International Neuropsychological Society 10, no. 2 (March 2004): 221–29. http://dx.doi.org/10.1017/s1355617704102087.

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The retrograde amnesia of patients with memory loss related to rupture and surgical repair of anterior communicating artery (ACoA) aneurysms is compared with the retrograde amnesia of temporal amnesic patients and nonamnesic control participants. Two tests which focus on popular culture but which differ according to extent of news exposure and the cognitive processes necessary for task performance were used to measure retrograde memory. ACoA patients demonstrated more significant retrograde memory problems than did nonamnesic controls; however, the severity and pattern of their memory loss was less severe than that seen in association with temporal amnesia. Different factors influenced the remote memory loss of respective groups: ACoA patients' problems were related to impaired lexical retrieval whereas temporal amnesic patients had problems secondary to both retrieval and storage deficits. (JINS, 2004, 10, 221–229.)

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Palmeri, Thomas J., and Marci A. Flanery. "Learning About Categories in the Absence of Training: Profound Amnesia and the Relationship Between Perceptual Categorization and Recognition Memory." Psychological Science 10, no. 6 (November 1999): 526–30. http://dx.doi.org/10.1111/1467-9280.00200.

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Previous evidence suggests that amnesics can categorize stimuli as well as normal individuals but are significantly worse at recognizing those stimuli. In an extreme case, a profoundly amnesic individual, E.P., was found to have near-normal categorization, yet, unlike most amnesics, was unable to recognize better than chance. This evidence has been used to argue against the possibility that a common memory system underlies these cognitive processes. However, we provide evidence that the experimental procedures typically used to test amnesic individuals may be flawed in that initial exposure to category members may be unnecessary to observe accurate categorization of test stimuli. We experimentally “induced” profound amnesia in normal individuals by telling them they had viewed subliminally presented stimuli, which were never actually presented. Using the same experimental paradigm used to test amnesics, we observed that participants' recognition performance was completely at chance, as should be expected, yet categorization performance was quite good.

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OSTERGAARD, ARNE L. "Priming deficits in amnesia: Now you see them, now you don't." Journal of the International Neuropsychological Society 5, no. 3 (March 1999): 175–90. http://dx.doi.org/10.1017/s1355617799533018.

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The rate with which perceptual information becomes available was manipulated in 2 word naming experiments. Word priming effects, in terms of reduced naming latencies for repeated items, and recognition memory measures were obtained with matched groups of amnesic patients and control participants. In both experiments, the amnesic patients evidenced significantly reduced priming effects compared to control participants under difficult task conditions. Under easy task conditions the baseline naming latencies of the amnesics were significantly longer than those of controls, but the difference in priming effects failed to reach significance. The findings are consistent with the Information Availability model of priming positing that both priming and explicit memory are mediated by episodic information from a study or information processing episode. It is argued that word priming does not represent a memory function that is spared in amnesia. (JINS, 1999, 5, 175–190.)

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8

Rickard, Timothy C., and Jordan Grafman. "Losing Their Configural Mind: Amnesic Patients Fail on Transverse Patterning." Journal of Cognitive Neuroscience 10, no. 4 (July 1998): 509–24. http://dx.doi.org/10.1162/089892998562915.

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A configural theory of human amnesia is proposed. The theory predicts that amnesic patients will exhibit selective deficits on tasks that normal subjects perform by learning new configurations of stimulus elements. This prediction is supported by results for four amnesic patients who learned a nonconfigural control task but failed to learn the configural transverse patterning task even after extensive practice. Matched normal subjects easily learned both tasks. The theory provides unique and viable accounts of the central results in the human amnesia literature. Relations between the configural approach and other theories are discussed.

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Kritchevsky, Mark, Joyce Zouzounis, and Larry R. Squire. "Transient global amnesia and functional retrograde amnesia: contrasting examples of episodic memory loss." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 352, no. 1362 (November 29, 1997): 1747–54. http://dx.doi.org/10.1098/rstb.1997.0157.

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We studied 11 patients with transient global amnesia (TGA) and 10 patients with functional retrograde amnesia (FRA). Patients with TGA had a uniform clinical picture: a severe, relatively isolated amnesic syndrome that started suddenly, persisted for 4−12 h, and then gradually improved to essentially normal over the next 12−24 h. During the episode, the patients had severe anterograde amnesia for verbal and non-verbal material and retrograde amnesia that typically covered at least two decades. Thirty hours to 42 days after the episode, the patients had recovered completely and performed normally on tests of anterograde and retrograde amnesia. By contrast, patients with FRA had a sudden onset of memory problems that were characterized by severe retrograde amnesia without associated anterograde amnesia and with a clinical presentation that otherwise varied considerably. The episodes persisted from several weeks to more than two years, and some of the patients had not recovered at the time of our last contact with them. The uniform clinical picture of TGA and the variable clinical picture of FRA presumably reflect their respective neurologic (‘organic’) and psychogenic (‘non-organic’) aetiologies.

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Potseluev, Sergey P. "On the Typology of Social Amnesia." Vestnik of Saint Petersburg University. Philosophy and Conflict Studies 39, no. 3 (2023): 557–68. http://dx.doi.org/10.21638/spbu17.2023.312.

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The purpose of the article is to clarify the concept of social amnesia, which often does not differ in modern research works from other manifestations of social forgetfulness. The author offers a general typology of this phenomenon, based on the conceptual distinctions introduced by T.Parsons and D.Easton. These refer to the difference between a social system and an actor, on the one hand, and the difference between a social group and grouping, on the other. Accordingly, the author identifies three types of social amnesia: systemic, structural, and actor one. The article draws attention to the difficulties of conceptualizing actor and structural amnesia, since they are often mixed with organized (prescribed) oblivion or the pragmatics of forgetting, complementing the process of memorization. To clarify these points, the author turns to the experience of studying the amnesic effects generated by the totalitarian organization of oblivion. To this end, the article analyzes the understanding of totalitarian amnesia in the artistic images of George Orwell, as well as in the concepts of Hannah Arendt that are consonant with them. The author emphasizes that the totalitarian “neuro-linguistic politics of memory” gives rise to amnesic effects regarding the past primarily in its living witnesses, and not only in future generations. Further, the author clarifies the concept of structural amnesia, which has received a contradictory interpretation in modern social sciences and humanities. In this regard, the article discusses the significant role of structural amnesia in the destruction but also in the formation of social identities. Based on the cases presented in the scientific studies to this topic, the author raises the question of the specifics of structural amnesia as an effect of social modernization and high mobility in the formation of national identities at micro- and macro-level.

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Saraf, Manish Kumar, Sudesh Prabhakar, Krishan Lal Khanduja, and Akshay Anand. "Bacopa monnieraAttenuates Scopolamine-Induced Impairment of Spatial Memory in Mice." Evidence-Based Complementary and Alternative Medicine 2011 (2011): 1–10. http://dx.doi.org/10.1093/ecam/neq038.

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Scopolamine, an anticholinergic, is an attractive amnesic agent for discerning the action of candidate antiamnesic drugs.Bacopa monnieraLinn (Syn. Brahmi) is one such antiamnesic agent that is frequently used in the ancient Indian medical system. We have earlier reported the reversal of diazepam-induced amnesia withB. monniera.In this study we wanted to test if scopolamine-induced impairment of spatial memory can also be ameliorated byB. monnierausing water maze mouse model. The objective of study was to study the effect ofB. monnieraon scopolamine-induced amnesia. We employed Morris water maze scale to test the amnesic effect of scopolamine and its reversal byB. monniera.Rotarod test was conducted to screen muscle coordination activity of mice. Scopolamine significantly impaired the acquisition and retrieval of memory producing both anterograde and retrograde amnesia.Bacopa monnieraextract was able to reverse both anterograde and retrograde amnesia. We propose thatB. monniera'seffects on cholinergic system may be helpful for developing alternative therapeutic approaches for the treatment of Alzheimer's disease.

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12

Meudell, P. R. "Irrelevant, Incidental and Core Features in the Retrograde Amnesia Associated with Korsakoff’s Psychosis: A Review." Behavioural Neurology 5, no. 2 (1992): 67–74. http://dx.doi.org/10.1155/1992/493789.

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A brief review of the literature on retrograde amnesia in Korsakoff's syndrome is presented. Various explanations of the phenomenon are discussed including the notions that it results from the effects of “state-dependency”, that it occurs as a result of a progressive learning problem and that it arises through a failure in contextual processing. None of these hypotheses can satisfactorily account for the length and temporal gradient of alcoholic amnesics retrograde amnesia. Although some evidence points towards the hypothesis that anterograde and retrograde amnesia might result from separate and independent impairments, this view is presently unproven and leaves open what causes the form and duration of Korsakoffs retrograde amnesia.

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Squire, Larry R., and Stuart M. Zola. "Amnesia, memory and brain systems." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 352, no. 1362 (November 29, 1997): 1663–73. http://dx.doi.org/10.1098/rstb.1997.0148.

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Bilateral damage to either the medial temporal lobe or the diencephalic midline causes an amnesic syndrome, i.e. a global impairment in the ability to acquire new memories regardless of sensory modality, and a loss of some memories, especially recent ones, from the period before amnesia began. The memory deficit can occur against a background of intact intellectual and perceptual functions. Two themes have been prominent in recent work. First, the amnesic syndrome is narrower than once believed in the sense that a number of learning and memory abilities are preserved (e.g. skill and habit learning, simple forms of conditioning and the phenomenon of priming). Second, the brain system damaged in amnesia has only a temporary role in memory. As time passes after learning, memory is reorganized and consolidated within neocortex, such that eventually medial temporal lobe and diencephalic structures are not needed for storage or retrieval.

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Rigby, Andrew. "Amnesty and Amnesia in Spain." Peace Review 12, no. 1 (March 2000): 73–79. http://dx.doi.org/10.1080/104026500113845.

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Zikmund, Ashlyn J., and James F. Briggs. "Post-extinction Delay Necessary to Induce Retrograde Amnesia for a Moderate Extinction Training Memory." Open Psychology Journal 9, no. 1 (July 29, 2016): 66–74. http://dx.doi.org/10.2174/1874350101609011866.

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Two experiments using rats were conducted to evaluate the post-extinction delay necessary to obtain retrograde amnesia for a moderate extinction training memory. In Experiment 1, six minutes of extinction (i.e., cue-exposure) was sufficient to reduce fear of the black compartment of a white-black shuttle box, however the amnestic treatment cycloheximide (CHX) failed to produce retrograde amnesia for extinction (i.e., show fear). In Experiment 2, CHX was administered at various post-extinction delays (0-min, 60-min, 75-min, 120-min) to assess whether the active extinction memory could be susceptible to amnesia if the original fear memory had time to reconsolidate. The results indicated that administrating CHX 75 minutes after extinction produced retrograde amnesia for extinction, but not for shorter post-extinction delays, thus demonstrating a temporal gradient. These findings suggest that the extinction memory was active and susceptible to disruption 75 minutes after the extinction session, but the original fear memory may have been protected from the amnestic effects with sufficient time to reconsolidate.

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16

Curran, Tim. "Higher-Order Associative Learning in Amnesia: Evidence from the Serial Reaction Time Task." Journal of Cognitive Neuroscience 9, no. 4 (July 1997): 522–33. http://dx.doi.org/10.1162/jocn.1997.9.4.522.

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Patients with anterograde amnesia are commonly believed to exhibit normal implicit learning. Research with the serial reaction time (SRT) task suggests that normal subjects can implicitly learn visuospatial sequences through a process that is sensitive to higher-order information that is more complex than pairwise associations between adjacent stimuli. The present research reexamined SRT learning in a group of amnesic patients with a design intended to specifically address the learning of higher-order information. Despite seemingly normal learning effects on average, the results suggest that amnesic patients do not learn higher-order information as well as control subjects. These results suggest that amnesic patients have an associative learning impairment, even when learning is implicit, and that the medial temporal lobe and/or diencephalic brain areas typically damaged in cases of amnesia normally contribute to implicit sequence learning.

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Angelini, R., F. Capozzoli, P. Lepore, D. Grossi, and A. Orsini. "“Experimental Amnesia” Induced by Emotional Items." Perceptual and Motor Skills 78, no. 1 (February 1994): 19–28. http://dx.doi.org/10.2466/pms.1994.78.1.19.

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Tulving described an effect of retrograde amnesia in a free-recall task of word lists, produced by inserting items having priority in recall. Other authors confirmed the amnesic effect without giving instructions for priority both in recall and in recognition tasks. The effect was explained by Tulving as a premature termination of encoding processes. The similarity between these experiments and the researches aimed at reproducing amnesia by emotional trauma led us to hypothesize that the two phenomena might be due to the same functional mechanisms. We have organized a free-recall task of word lists into which emotional items were inserted. Our aim was to verify whether with these experimental conditions Tulving's results would be reproduced. The obtained data show amnesic effects in free recall; nevertheless, they do not seem to confirm closely the experimental hypothesis. Lastly, changes in primacy and recency effects produced by emotional items are analyzed.

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Ramos, S. Freitas, M. Seabra, P. Â. Horta, J. Guimarães, and R. Grangeia. "A blank slate – apropos a clinical case." European Psychiatry 64, S1 (April 2021): S648. http://dx.doi.org/10.1192/j.eurpsy.2021.1722.

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IntroductionDissociative Amnesia remains an enigmatic and controversial entity. It is classically described as responsible for autobiographic amnesia associated with a traumatic event.ObjectivesTo report a clinical case and review the literature.MethodsWe collected data from the patient’s clinical file with his informed consent. We conducted a non-systematic review of the literature.ResultsA 46-years-old patient presents to the emergency department for sudden global retrograde amnesia, with multiple domain amnestic syndrome (impairing verbal and visual memory, processing speed, mental flexibility, calculus, executive functions and language). He was initially admitted for a suspected infectious meningoencephalitis, which was not confirmed. Later an autoimmune encephalitis was pursued. Brain MRI showed a nonspecific left temporal and hipocampal hyperintensity and the EEG a mild left temporal dysfunction. The autoimmune encephalitis panel was negative and the formal diagnostic criteria were not met. The neurologic examination at discharge presented only with autobiographical and semantic amnesia. On the mental state examination, he presented with depressive symptoms reactive to the situation. There was no evident traumatic event apart from a promotion received the day before the amnesia started. He was prescribed escitalopram 10 mg/day. The amnesia was maintained at 9 months follow-up.ConclusionsOur case report illustrates a case of amnesia without evident organic or psychogenic cause, assumed as a dissociative amnesia. Further studies are necessary to clarify the pathophysiology of this condition and develop specific treatments.DisclosureNo significant relationships.

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Wagner, BK, DA O'Hara, and JS Hammond. "Drugs for amnesia in the ICU." American Journal of Critical Care 6, no. 3 (May 1, 1997): 192–201. http://dx.doi.org/10.4037/ajcc1997.6.3.192.

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OBJECTIVE: This review focuses on how patients' recall of their stay in the ICU can be modified pharmacologically. DATA SOURCES: Computerized MEDLINE and PAPERCHASE searches of English- and foreign-language published research from 1966 to 1995, bibliographies, pharmaceutical and personal files, and conference abstract reports. STUDY SELECTION: All abstracts from uncontrolled and controlled clinical trials were reviewed. DATA EXTRACTION: Study design, population, results, and safety information were retained. Efficacy conclusions were drawn from controlled trials. DATA SYNTHESIS: Patients without cerebral injury may recall mental and physical discomfort during their stay in the ICU. All benzodiazepines produce amnestic effects, but the short duration of action, lack of long-acting metabolites, and potent amnestic effects make lorazepam and midazolam preferable in this setting. Infusions of propofol for conscious sedation produce concentrations below those required for consistent amnesia. Opioids generally do not produce amnesia; however, end-organ failure and use of high doses of opioids may increase plasma concentrations to levels that produce impairment of learning and various degrees of amnesia. High infusion rates of ketamine may be required for satisfactory amnesia and pain control (with coadministration of benzodiazepine). Barbiturates and haloperidol do not impair memory in patients who are not critically ill. Antihistamines and anticholinergics that do not penetrate the central nervous system do not produce amnesia. Flumazenil may induce recall. CONCLUSIONS: Patients may remember their stay in the ICU, depending on the type of injury and the drug therapy. Of the drugs presented, benzodiazepines most reliably provide anterograde amnesia, whereas ketamine and propofol exhibit dose-dependent effects on memory.

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Millar, Keith, William J. Jeffcoate, and Cristine P. Walders. "Vasopressin and memory: improvement in normal short-term recall and reduction of alcohol-induced amnesia." Psychological Medicine 17, no. 2 (May 1987): 335–41. http://dx.doi.org/10.1017/s0033291700024879.

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SynopsisThe vasopressin analogue 1-desamino-8-D-arginine vasopressin (DDAVP) has been shown in healthy male volunteers to cause significant improvement in short-term memory and to reduce alcohol-induced amnesia. There was no significant effect upon semantic retrieval or simple reaction time. It was concluded that vasopressin benefited the initial processes of consolidation and learning, while the reduction of the amnesic effects of alcohol may support the contentions of other authors that the peptide improves memory in states of mild amnesia.

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Keane, Margaret M., John D. E. Gabrieli, Julia S. Noland, and Susan Ingemanson McNealy. "Normal perceptual priming of orthographically illegal nonwords in amnesia." Journal of the International Neuropsychological Society 1, no. 5 (September 1995): 425–33. http://dx.doi.org/10.1017/s1355617700000527.

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AbstractThis study examined priming in perceptual identification of orthographically illegal nonwords in control subjects and patients with global amnesia. Subjects studied a list of orthographically illegal nonwords and then performed a perceptual identification task in which half of the stimuli were from the prior study list and half were new (unstudied) stimuli. Priming was reflected in enhanced identification accuracy of studied compared to unstudied nonwords. Amnesic patients showed significant and normal priming despite impaired recognition memory performance. Because the experimental stimuli were dissimilar to real words in terms of orthography and phonology, it is unlikely that this priming effect was mediated by activation of pre-existing representations of orthographically or phonologically similar words, morphemes, or syllables. These results demonstrate that intact perceptual priming in amnesia is not limited to stimuli that are premorbidly represented in long-term knowledge, nor to novel stimuli that conform to the rules that characterize familiar items. Further, because the experimental stimuli comprised novel letter assemblies, the results suggest that amnesic patients can show normal priming for new perceptual associations. These findings demonstrate that processes spared in amnesia can support the creation and subsequent retrieval of novel stimulus representations. (JINS, 1995, I, 425–433.)

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Lipatova, L. V., I. V. Sakovsky, and M. B. V. Gadaborshev. "Transient epileptic amnesia versus transient global amnesia: aspects of differential diagnosis." Epilepsy and paroxysmal conditions 16, no. 2 (June 30, 2024): 137–44. http://dx.doi.org/10.17749/2077-8333/epi.par.con.2024.185.

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Transient global amnesia (TGA) and transient epileptic amnesia (TEA) are rare phenomena in clinical practice that manifest as transient cognitive amnestic impairments. Despite the similarity in clinical picture, such conditions are pathogenetically heterogeneous and require different therapeutic approaches. TGA is a clinical syndrome characterized by sudden anterograde amnesia of the event lasting up to 24 hours, lacking focal neurological symptoms, and not prone to recurrence. Mimicking TGA, TEA often occurs manifested as epileptic seizures with impaired awareness of varying duration, including long-term (more than 24 hours), as a variant of focal epilepsy. TEA is characterized by recurrent episodes, combination with other manifestations of epilepsy, and comorbidity with neurodegenerative diseases (dementia). For differential diagnosis, it is necessary to use prolonged video-electroencephalographic monitoring with sleep recording, neuroimaging methods (brain magnetic resonance imaging, positron emission tomography), psychological testing, biochemical examination for markers of neurodegeneration.

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Adedayo, Lawrence, Godgift Offor, Olalekan Jolayemi, Gideon Ojo, Olubayode Bamidele, Alaba Ojo, Timothy Emmanuel, Nimedia Aitokhuehi, Samuel Onasanwo, and Abiodun Ayoka. "Aripiprazole ameliorates scopolamine-induced amnesia in mice." Journal of Pharmacy & Bioresources 18, no. 1 (May 28, 2021): 12–24. http://dx.doi.org/10.4314/jpb.v18i1.2.

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Aripiprazole, a known third generation anti-psychotic drug. The drug has shown to have lesser side effects on extrapyramidal system and enhance memory when compared with the first-generation anti-psychotic drugs. However, studies on the impact of aripiprazole on scopolamine-induced memory impairment in mice have been poorly reported. This study was designed to investigate the impact of aripiprazole on scopolamine-induced amnesia in mice. Thirtysix (36) mice weighing between 20-23g were randomly divided into six groups. Group 1 was given 10 ml/kg distilled water. Group 2 received 3 mg/kg scopolamine alone. Group 3 was given 1 mg/kg donepezil. Group 4 received 0.5 mg/kg aripiprazole. Group 5 was given 0.3 mg/kg aripiprazole. Group 6 received 0.1mg/kg aripiprazole. Thirty minutes after administration of either aripiprazole or donepezil, scopolamine (3 mg/kg) was administered, intraperitoneally. The administration was for 7days, during which their memory was assessed using Morris water maze and Y-maze models. The results showed that the anti-amnesic effect of aripiprazole appeared to be dosedependent; the animals administered with 0.5 mg/kg aripiprazole showed the greatest improved memory performance against scopolamine-induced amnesia. The hippocampal and prefrontal cortex tissues displayed anti-amnesic potential of aripiprazole. Aripiprazole seems to improved memory performance against scopolamine-induced memory impairment in mice. Keywords: Aripiprazole; Anti-amnesic; Scopolamine; Memory

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Knott, Raymond, and William Marslen-Wilson. "Does the Medial Temporal Lobe Bind Phonological Memories?" Journal of Cognitive Neuroscience 13, no. 5 (July 1, 2001): 593–609. http://dx.doi.org/10.1162/089892901750363181.

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The medial temporal lobes play a central role in the consolidation of new memories. Medial temporal lesions impair episodic learning in amnesia, and disrupt vocabulary acquisition. To investigate the role of consolidation processes in phonological memory and to understand where and how, in amnesia, these processes begin to fail, we reexamined phonological memory in the amnesic patient HM. While HM's word span performance was normal, his supraspan recall was shown to be markedly impaired, with his recall characterized by a distinctive pattern of phonological errors, where he recombined phonemes from the original list to form new response words. These were similar to errors observed earlier for patients with specifically semantic deficits. Amnesic Korsakoff's patients showed a similar, though much less marked, pattern. We interpret the data in terms of a model of lexical representation where temporal lobe damage disrupts the processes that normally bind semantic and phonological representations.

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Allen, Richard J. "Classic and recent advances in understanding amnesia." F1000Research 7 (March 16, 2018): 331. http://dx.doi.org/10.12688/f1000research.13737.1.

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Neurological amnesia has been and remains the focus of intense study, motivated by the drive to understand typical and atypical memory function and the underlying brain basis that is involved. There is now a consensus that amnesia associated with hippocampal (and, in many cases, broader medial temporal lobe) damage results in deficits in episodic memory, delayed recall, and recollective experience. However, debate continues regarding the patterns of preservation and impairment across a range of abilities, including semantic memory and learning, delayed recognition, working memory, and imagination. This brief review highlights some of the influential and recent advances in these debates and what they may tell us about the amnesic condition and hippocampal function.

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Na, Seunghee, Eek-Sung Lee, and Seung-Jae Lee. "Transient Global Amnesia in a Patient with Pituitary Adenoma: Causal or Chance Association?" Case Reports in Neurology 11, no. 2 (August 16, 2019): 238–41. http://dx.doi.org/10.1159/000502086.

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A 65-year-old man with no underlying medical history visited the neurology department due to transient amnesia lasting for about 8 h. During the amnesia episode, he was alert but showed repetitive questioning. The episode fulfilled the diagnostic criteria for transient global amnesia (TGA). On workups for excluding alternative diagnoses, the brain magnetic resonance imaging revealed a 3 × 6 cm-sized hemorrhagic pituitary tumor extending to the left medial temporal lobe and anterior hippocampus. The electroencephalogram revealed intermittent slowing in the left temporal region with normal backgrounds. The tumor was surgically removed and pathologically proven to be a nonfunctioning adenoma. At 6 months postoperatively, no complication or new amnestic episode occurred. Thus, our case had a typical TGA as the first manifestation of a pituitary tumor. There were no features of epileptic amnesia. Transiently altered flow status from a mass effect in the memory-eloquent area might be the possible pathogenic mechanism underlying the TGA though there still remains a probability of chance concurrence of TGA and tumor.

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KISSLER, JOHANNA, and KARL-HEINZ BÄUML. "Memory retrieval in schizophrenia: Evidence from part-list cuing." Journal of the International Neuropsychological Society 11, no. 3 (May 2005): 273–80. http://dx.doi.org/10.1017/s1355617705050320.

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Schizophrenia patients are known to exhibit episodic verbal memory deficits. Although their neural origin is debated, they have often been compared to the memory problems found in temporal lobe amnesia or frontal lobe dysfunction. Furthermore, it is unclear to what extent such deficits arise at either memory encoding or retrieval. We addressed the issue of retrieval deficits in schizophrenia in a part-list cuing experiment, testing the effect of the presentation of a subset of previously learned material on the retrieval of the remaining items. The part-list cuing procedure generally impairs retrieval but previous work showed that the detrimental effects are more pronounced in amnesic participants than in healthy people, indicating a retrieval deficit under part-list cuing conditions in amnesia. In the present study, schizophrenia patients did not exhibit increased susceptibility to part-list cuing effects and thus showed no increased retrieval inhibition from part-list cuing. Moreover, in part-list cuing, schizophrenia patients did not mirror the pattern found in amnesia, demonstrating a dissociation between amnesia and schizophrenia patients with respect to this particular memory effect. Implications for the neural basis of the part-list cuing effect and of memory disturbances in schizophrenia are discussed. (JINS, 2005, 11, 273–280.)

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Alkire, Michael T., and Sheila V. Nathan. "Does the Amygdala Mediate Anesthetic-induced Amnesia?" Anesthesiology 102, no. 4 (April 1, 2005): 754–60. http://dx.doi.org/10.1097/00000542-200504000-00010.

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Background Amnesia for aversive events caused by benzodiazepines or propofol depends on the basolateral amygdala (BLA). Whether the amnesia of volatile anesthesia is also mediated through the BLA is unknown. If so, a general principle of anesthetic-induced amnesia may be emerging. Here, using an inhibitory avoidance paradigm, the authors determine whether BLA lesions prevent sevoflurane-induced amnesia. Methods Male Sprague-Dawley rats were separated into two groups: sham-operated controls (n = 22) and rats given bilateral N-methyl-D-aspartate lesions of the BLA (n = 32). After a 1-week recovery, the rats were randomly assigned to be trained during either air or sevoflurane (0.3% inspired, 0.14 minimum alveolar concentration) exposure. Animals learned to remain in the starting safe compartment of a step-through inhibitory avoidance apparatus for 100 consecutive seconds by administering foot shock (0.3 mA) whenever they entered an adjacent shock compartment. Memory was assessed at 24 h. Longer latencies to enter the shock compartment at 24 h imply better memory. Results Sham-air (n = 10) animals had a robust memory, with a median retention latency of 507 s (interquartile range, 270-600 s). Sham-sevoflurane (n = 6) animals were amnesic, with a latency of 52 s (27-120 s) (P < 0.01, vs. sham-air). Both the air-exposed (n = 5) and the sevoflurane-exposed (n = 8) animals with BLA lesions showed robust memory, with latencies of 350 s (300-590 s) and 378 s (363-488 s), respectively. The latencies for both did not differ from the performance of the sham-air group and were significantly greater than the latency of the sham-sevoflurane group (both P < 0.01). Conclusions BLA lesions block sevoflurane-induced amnesia. A role for the BLA in mediating anesthetic-induced amnesia may be a general principle of anesthetic action.

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AGOSTI, CHIARA, BARBARA BORRONI, NABIL AKKAWI, and ALESSANDRO PADOVANI. "Three sisters covering the transient global amnesia spectrum." International Psychogeriatrics 19, no. 5 (June 13, 2007): 987–89. http://dx.doi.org/10.1017/s1041610207005637.

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We report the case of an Italian family in which three sisters experienced transient global amnesia (TGA). Since its early description, this transitory pure memory deficit has attracted increasing interest, especially within the neurological community. In 1964 the term “TGA” was coined to identify the abrupt onset of anterograde amnesia, accompanied by repetitive queries lasting for hours and then gradually recovering, leaving an amnesic gap for the duration of the attack. Afterwards, many studies focused on TGA, and in 1990 clinical criteria were defined by Hodges and Warlow (1990). Further studies showed that meeting diagnostic criteria was a significant predictor for a better outcome than in other forms of transient amnesia, while amnesic patients who did not fulfil the TGA criteria had different outcomes. Precipitating and trigger events for TGA were identified and divided into physical and psychological factors (Inzitari et al., 1997; Quinette et al., 2006). Physical precipitants were found to be gardening, housework and sawing wood, contact with water and changes in body temperature occurring during hot baths or showers, or a cold swim at the swimming pool. Emotional trigger events included a major life or death event, emotional stress triggered by a gastric endoscopy, an exhausting work session, and anxiety resulting from conflicts at home or at work, health problems and money worries. Several hypotheses have been proposed for its pathogenesis such as psychogenic, venous dysfunction due to jugular venous valve incompetence, or ischemic aetiology, but the enigma of TGA still needs to be unravelled (Lewis, 1998; Akkawi et al., 2001).

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Fazio, Ferruccio, Daniela Perani, Maria Carla Gilardi, Fabio Colombo, Stefano F. Cappa, Giuseppe Vallar, Valentino Bettinardi, et al. "Metabolic Impairment in Human Amnesia: A PET Study of Memory Networks." Journal of Cerebral Blood Flow & Metabolism 12, no. 3 (May 1992): 353–58. http://dx.doi.org/10.1038/jcbfm.1992.52.

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Human amnesia is a clinical syndrome exhibiting the failure to recall past events and to learn new information. Its “pure” form, characterized by a selective impairment of long-term memory without any disorder of general intelligence or other cognitive functions, has been associated with lesions localized within Papez's circuit and some connected areas. Thus, amnesia could be due to a functional disconnection between components of this or other neural structures involved in long-term learning and retention. To test this hypothesis, we measured regional cerebral metabolism with 2-[18F]fluoro-2-deoxy-d-glucose ([18F]FDG) and positron emission tomography (PET) in 11 patients with “pure” amnesia. A significant bilateral reduction in metabolism in a number of interconnected cerebral regions (hippocampal formation, thalamus, cingulate gyrus, and frontal basal cortex) was found in the amnesic patients in comparison with normal controls. The metabolic impairment did not correspond to alterations in structural anatomy as assessed by magnetic resonance imaging (MRI). These results are the first in vivo evidence for the role of a functional network as a basis of human memory.

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Tate, Robyn L., and Anne Pfaff. "Problems and Pitfalls in the Assessment of Posttraumatic Amnesia." Brain Impairment 1, no. 2 (October 1, 2000): 116–29. http://dx.doi.org/10.1375/brim.1.2.116.

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AbstractIn the early stages of recovery after a traumatic brain injury, patients usually experience a period of posttraumatic amnesia (PTA) in which they are confused, amnesic for ongoing events, and frequently behaviourally agitated. Although a variety of procedures and instruments are available to measure the duration of PTA, their applications in clinical practice are far from ideal. This review paper describes retrospective and prospective measures of PTA and critically examines variations in item content and scoring procedures. In particular, methods currently available to measure the amnesia component of PTA are especially problematic. The limitations of PTA scales give rise to a number of difficulties that impact upon clinical practice. These include determining precisely when a patient has emerged from PTA, and distinguishing between patients in PTA and those with chronic amnesia. It is concluded that there is a need to revisit basic constructs comprising PTA, and develop an instrument with greater specificity. More focus should be placed on examining the confusional component of PTA, and validity of PTA tests would be improved by measuring attention and behaviour, in addition to orientation and memory.

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Lisichenko, I. A., V. G. Gusarov, B. A. Teplykh, N. V. Chayanov, and M. N. Zamyatin. "Assessment of Amnesic Effect and the Depth of Hypnosis During Therapeutic Inhalation of Xenon-Oxygen Mixture." Messenger of ANESTHESIOLOGY AND RESUSCITATION 19, no. 5 (October 28, 2022): 19–27. http://dx.doi.org/10.21292/2078-5658-2022-19-5-19-27.

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The current literature lacks data on the incidence of intraoperative awakening during xenon anesthesia. This could be due to amnesia preventing memories of the intraoperative awakening.The objective: to determine the concentration of xenon in the xenon-oxygen mixture, which causes amnesia for events during inhalation in 100% of patients, and to make correlations with the depth of hypnosis as per Kugler scale.Subjects and Methods: 34 patients with chronic neurogenic pain who received 111 20-minute inhalations with concentration of xenon up to 50% were included in the study. Amnesia evaluation, EEG monitoring, and pain assessment on a visual analog scale (VAS) were performed.Results. Amnesic effect developed in 100% of patients at xenon concentration of 45%. On inhalation of xenon at concentrations of up to 50%, EEG changes did not exceed D1 grade on Kugler scale. The decrease in bispectral index (BIS) did not reach the level of deep sedation (Me 96.2%) at xenon concentration of 50%. The decrease in pain on VAS was approximately 60%.Conclusions. Xenon inhalations cause transient congradic amnesia at concentrations of 45% or more. The accuracy of the BIS monitoring readings may be reduced when using xenon in a monovariant. Inhalations of xenon-oxygen mixture in concentrations up to 50% showed good analgesic properties in the framework of combined therapy of chronic pain syndrome.

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Barbeau, Emmanuel J., Mira Didic, Olivier Felician, Eve Tramoni, Eric Guedj, Mathieu Ceccaldi, and Michel Poncet. "Pure progressive amnesia: An atypical amnestic syndrome?" Cognitive Neuropsychology 23, no. 8 (December 2006): 1230–47. http://dx.doi.org/10.1080/02643290600893594.

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Prather Palmer, E. "Transient Global Amnesia and the Amnestic Syndrome." Medical Clinics of North America 70, no. 6 (November 1986): 1361–74. http://dx.doi.org/10.1016/s0025-7125(16)30904-x.

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Kixmiller, Jeffrey S., Mieke Verfaellie, Kenneth A. Chase, and Laird S. Cermak. "Comparison of figural intrusion errors in three amnesic subgroups." Journal of the International Neuropsychological Society 1, no. 6 (November 1995): 561–67. http://dx.doi.org/10.1017/s1355617700000692.

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AbstractTo examine the contribution of memory deficits and executive dysfunction to the production of prior-item intrusion errors, Korsakoff, mesial temporal amnesic, and anterior communicating artery aneurysm (ACoA) patients’ performance on the Visual Reproduction subtest of the Wechsler Memory Scale-Revised (WMS-R) was assessed. The Korsakoff patients were matched to the mesial temporal group in terms of severity of amnesia, while the ACoA group, which was less severely amnesic, was matched to the Korsakoff group in their performance on executive tests. Results indicated that at immediate recall, Korsakoff patients made significantly more intrusions than mesial temporal and ACoA patients. Conversely, after a delay, ACoA patients tended to make more intrusions than the other groups. Findings suggest that intrusions are due to a combination of deficient memory and executive dysfunction. A further comparison of a subgroup of ACoA patients matched to the Korsakoff patients in terms of severity of amnesia, however, revealed differences in the pattern of intrusions of these two groups, suggesting that different mechanisms may underlie Korsakoff and ACoA patients’ susceptibility to interference. (JINS, 1995, 1, 561–567.)

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Stöllberger, Claudia, Julia Koller, Josef Finsterer, Dominic Schauer, and Marek Ehrlich. "Anterograde Amnesia as a Manifestation of Acute Type A Aortic Dissection." International Journal of Angiology 29, no. 04 (July 5, 2019): 263–66. http://dx.doi.org/10.1055/s-0039-1693029.

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Objectives Memory impairment has been only rarely reported in association with acute aortic dissection type A. We report a patient with pure anterograde amnesia and memory impairment of contents occurring after the event, accompanying acute aortic dissection type A. Case Report A previously healthy 53-year-old Caucasian male was admitted because of sudden chest pain after having lifted a heavy object. Clinical examination and electrocardiogram showed no abnormalities. Since blood tests showed leukocytosis, anemia, and elevated D-dimer level, either pulmonary embolism or aortic dissection was suspected; therefore, computed tomography was suggested. The patient seemed disoriented to time, and neurologic investigation confirmed that the patient was disoriented to time; short time memory was severely impaired and concentration was reduced. An amnestic episode with anterograde amnesia was diagnosed. Computed tomography showed type A aortic dissection. A supracoronary replacement of the ascending aorta was performed. The patient was discharged on the 7th postoperative day. Three months postoperatively, the patient is clinically stable; however, amnesia for the interval between pain onset and cardiac surgery persists. Conclusions Transient amnesia, usually considered a benign syndrome, may be more common than generally recognized in aortic dissection. The suspicion for aortic dissection or other cardiovascular emergencies is substantiated when amnesia is associated with sudden onset of chest pain, leukocytosis, and elevated D-dimer levels. Computed tomography of the aorta with contrast medium is the imaging method of choice to confirm or exclude the diagnosis.

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Gordon Hayman, C. A., Carol A. Macdonald, and Endel Tulving. "The Role of Repetition and Associative Interference in New Semantic Learning in Amnesia: A Case Experiment." Journal of Cognitive Neuroscience 5, no. 4 (October 1993): 375–89. http://dx.doi.org/10.1162/jocn.1993.5.4.375.

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The question of whether globally amnesic subjects can learn new semantic (factual) information is controversial. Some students of amnesia believe that they can, others that they cannot. In this article we report an extensive experiment conducted with the amnesic patient K.C. in which we examined the role of repetition and associative interference in his learning of new semantic information. In the course of 8 study sessions distributed over 4 weeks, we taught K.C. novel, amusing definitions of 96 target words (e.g., “a talkative featherbrain—PARAKEET”). We varied systematically the degree of both pre-experimental and intraexperimental associative interference, as well as the amount of study. The results of the experiment showed that K.C. can learn new semantic knowledge, and retain it over a period as long as 30 months indistinguishably from control subjects. The results further showed that the efficacy of such learning depends critically on both repetition of the material and the absence, or minimization, of pre-experimental and intraexperimental associative interference. These findings suggest that the extent to which at least some amnesic patients can acquire and retain new semantic knowledge depends on the conditions under which learning occurs, and that unqualified statements regarding the deficiency or absence of such learning in amnesia are not justified.

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Kumar, Dinesh, Asheesh K. Gupta, Navneet Verma, and Sushil Kumar. "Evaluation of Anti-amnesic Activity of Ethanolic Extract of Averrhoa carambola Leaves." INTERNATIONAL JOURNAL OF PHARMACEUTICAL QUALITY ASSURANCE 15, no. 01 (March 25, 2024): 421–28. http://dx.doi.org/10.25258/ijpqa.15.1.65.

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The current research aims to screen the anti-amnesic and neuroprotective efficacy of ethanolic extract of Averrhoa carambola (EEAC) leaves. To fulfill the above purpose, phytochemical screening, quantity of total phenolic, flavonoids, behavioral study, biochemical study and histopathological study were performed. The results of phytochemical screening, quantities of total phenolic flavonoids, behavioral study, biochemical study and histopathological studies revealed the anti-amnesic and neuroprotective activity of the EEAC. EEAC shows anti-amnesic and neuroprotective activity due to numerous phytoconstituents and high amounts of phenolic and flavonoids. The results of this study show that the EEAC may be useful for managing amnesia.

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Yasnetsov, Victor V., Diana E. Kaurova, Sofia Ya Skachilova, and Evgeniy Yu Bersenev. "Antiamnestic effect of new nicotinic acid derivatives." Research Results in Pharmacology 7, no. 3 (September 7, 2021): 15–22. http://dx.doi.org/10.3897/rrpharmacology.7.68001.

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Introduction: The search for new drugs for the prevention and treatment of vascular cognitive disorders continues to be a relevant task of pharmacology. In this regard, the aim of this work is to study the antiamnestic effect of five new nicotinic acid derivatives in comparison with the well-known drug mexidol (ethylmethylhydroxypyridine succinate) in animals. Materials and methods: The experiments were carried out on white male mice using conditioned passive avoidance reflex (CPAR). Electroconvulsive shock (ECS), scopolamine administration, and acute hypoxia in a hermetic chamber were used as amnesic effects. Testing for the safety of CPAR was performed 24 h after amnesic exposure. The new substances, reference drug mexidol, and a 0.9% sodium chloride solution (control group) were administered once intraperitoneally 60 min before mice training. Results and discussion: Three of the five new nicotinic acid derivatives, LKhT 4-19 (100 mg/kg), LKhT 6-19 (25, 50, and 100 mg/kg), and LKhT 7-19 (100 mg/kg), have antiamnestic properties on models of amnesia in mice induced by ESC, scopolamine, and acute hypoxia in a hermetic chamber. At the same time, the most efficient substance – LKhT 6-19 – exceeds the reference drug mexidol on all three models used. In addition, this compound is also more efficient than two other new compounds, LKhT 4-19 and LKhT 7-19, on the model of ESC-induced amnesia and LKhT 7-19 on the scopolamine-induced amnesia model. Conclusion: Compound LKhT 6-19 is promising for further advanced preclinical studies as a potential drug with antiamnestic activity. Graphical abstract:

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Laurent, B., R. F. Allegri, C. Thomas-Anterion, N. Foyatier, B. Naegele-Faure, and J. Pellat. "Long Term Neuropsychological Follow-Up in Patients With Herpes Simplex Encephalitis and Predominantly Left-Sided Lesions." Behavioural Neurology 4, no. 4 (1991): 211–24. http://dx.doi.org/10.1155/1991/432895.

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Five patients with predominantly dominant cerebral hemisphere lesions due to herpes simplex encephalitis are described. Verbal amnesia was the main deficit but amnesic aphasia sometimes associated with impairment of remote memory also occurred. Semantic and episodic memory deficits were also explored in one case and the role of the right cerebral hemisphere in facilitating recovery of learning is discussed.

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Farrell, Michael. "Amnesia." Antipodes 32, no. 1-2 (2018): 74–75. http://dx.doi.org/10.1353/apo.2018.0008.

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Wakutani, Yosuke. "Amnesia." Nihon Naika Gakkai Zasshi 103, no. 5 (2014): 1214–18. http://dx.doi.org/10.2169/naika.103.1214.

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Frey, John. "Amnesia." British Journal of General Practice 61, no. 583 (February 1, 2011): 150–51. http://dx.doi.org/10.3399/bjgp11x556416.

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Farrell. "Amnesia." Antipodes 32, no. 1-2 (2018): 74. http://dx.doi.org/10.13110/antipodes.32.1-2.0074.

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Pearce, J. M. S. "Amnesia." European Neurology 57, no. 2 (December 18, 2006): 126. http://dx.doi.org/10.1159/000098103.

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Benson, Neil. "Amnesia." Neurology Now 4, no. 4 (July 2008): 5. http://dx.doi.org/10.1097/01.nnn.0000333828.73364.11.

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&NA;. "Amnesia." Neurology Now 4, no. 4 (July 2008): 5. http://dx.doi.org/10.1097/01.nnn.0000333829.80988.0a.

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Shrager, Yael, and Larry Squire. "Amnesia." Scholarpedia 3, no. 8 (2008): 2789. http://dx.doi.org/10.4249/scholarpedia.2789.

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Rogers, Richard, and James L. Cavanaugh. "Amnesia." Behavioral Sciences & the Law 4, no. 1 (1986): 1–3. http://dx.doi.org/10.1002/bsl.2370040101.

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Cording, Robert. "Amnesia." Spiritus: A Journal of Christian Spirituality 10, no. 2 (September 2010): 305–6. http://dx.doi.org/10.1353/scs.2010.a403009.

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Journal articles on the topic 'Amnesia'

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