Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “AMNESIA”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 379 records · Page 21Linked to original sources

Psychogenic amnesia.

Time- and content-based memory systems are briefly described so that their importance for a refined analysis of memory disturbances becomes evident. These memory systems are then related to their brain instantiation, emphasizing that there are limbic circuits for encoding different forms of memories, largely cortical networks for memory storage, and a combined temporofrontal network acting to trigger information retrieval. The terms functional amnesias and psychogenic amnesias are discussed and their symptomatology is compared to that of organic amnesias. The term "mnestic block syndrome" is introduced and defined as a syndrome of its own. Experimental data, obtained especially with functional imaging methods, are presented to elucidate changes in neural activation during functional amnesic states. It is concluded that functional amnesic states, confined to a patient's biography, can be triggered by environmentally induced stress and trauma, leading to lasting inability to retrieve autobiographical events. Such an impairment may be identified at the brain level using functional imaging techniques.

Amnesia↗

Processing and short-term retention of relational information in amnesia.

In a recent eye-movement study [Psychol. Sci. 11 (2000) 454], amnesic patients failed selectively to exhibit long-term effects of memory for the relations among the constituent elements of scenes. This failure could be due to a deficit specifically in long-term relational memory, as we have suggested; or in retention of relational information over any delay, whether involving perceptual processing and short-term maintenance or long-term memory, consistent with suggestions from recent studies of the hippocampus; or in on-line processing of relational information, as would occur in perceptual or feature binding. Here we show robust eye-movement effects of relations among elements of scenes in amnesia in a short-delay matching task, with the same materials and in the same amnesic patients in which long-delay conditions elicited failure. These findings document intact processing and short-term retention of relational information in amnesia, indicating that amnesia associated with hippocampal damage results in a relational memory deficit, specifically of long-term memory.

Amnesia↗

Remembering and forgetting of semantic knowledge in amnesia: a 16-year follow-up investigation of RFR.

We report our long-term follow-up investigations of RFR, a post-encephalitic case of very grave anterograde and retrograde amnesia. We also describe the results of quantitative neuroimaging of his brain injury that showed bilateral and severe reduction in the hippocampal formation and medial temporal structures with sparing of left lateral/posterior and right posterior temporal cortex. We established that RFR had a persistent severe anterograde and retrograde amnesia for personal and public events. His personal semantic knowledge was relatively spared for the retrograde period. There was a modest and global reduction in RFR's vocabulary for words acquired in adulthood before he became amnesic but there was no evidence of any retrograde gradient. His retrograde knowledge of people was also without any gradient. Remarkably, there had been no change in the extent of his semantic knowledge across a prolonged re-test interval indicating that the loss of semantic knowledge was stable and likely to have arisen at the time of his initial lesion. RFR also showed evidence of a limited but significant ability to acquire new word meanings and a more restricted capacity for learning about new celebrities. While he was able to demonstrate face and name familiarity for newly famous people, he was unable to provide much semantic detail. RFR's amnesia can be partially explained by contemporary theories that allow for parallel cortical and hippocampal memory systems but is difficult to reconcile in detail with any extant view.

Aged↗

The relationship between working memory and episodic memory disorders in transient global amnesia.

In a previous study, we investigated the relationship between the disorders of both episodic memory and working memory in the acute phase of transient global amnesia (TGA). Since executive functions were spared, another dysfunction may be responsible for the binding and maintenance of multimodal informations and contribute to the encoding disorders observed in some patients [Quinette, P., Guillery, B., Desgranges, B., de la Sayette, V., Viader, F., & Eustache, F. (2003). Working memory and executive functions in transient global amnesia. Brain, 126, 1917-1934.]. The aim of this present study was to assess the functions of binding and maintenance of multimodal information during TGA and explore their involvement in episodic memory disorders. We therefore conducted a more thorough investigation of working memory in 16 new patients during the acute phase of TGA using two tasks designed to assess the binding process and both dimensions of the maintenance, namely the active storage and the memory load ability. We also investigated the nature of the episodic memory impairment in distinguishing between the performance of patients with preferential encoding deficits and those of patients with preferential storage disorders on the episodic memory task. This distinction was closely related to the severity of amnesia, i.e. an encoding disorder was observed rather in the early phase of TGA. The results showed that while the functions of binding and maintenance of multimodal information were intact in patients with storage disorders, they were impaired in the case of encoding deficits. These results are interpreted in the recent framework of episodic buffer proposed by Baddeley [Baddeley, A. D. (2000). The episodic buffer: A new component of working memory? Trends in Cognitive Sciences, 4, 417-423] that represents an interface between working memory and episodic memory.

Aged↗

Transient global amnesia triggered by the intracarotid amobarbital procedure.

The emergence of a sudden, global, and fully reversible amnestic state during an intracarotid amobarbital procedure (IAP) performed in a patient with a right temporal tumor is described. Forms of amnesia during the IAP are discussed, and it is argued that because of its appearance, the associated behavioral abnormalities, and EEG findings, this state was a transient global amnesia (TGA). In addition to other origins such as bitemporal lesions, increased barbiturate levels, seizures, and epileptic amnesia, TGA may triggered by stress or angiography during the IAP.

Adult↗

Pure retrograde amnesia following a mild head trauma: a neuropsychological and metabolic study.

After a minor closed head injury, a 33-year-old man acquired extensive retrograde amnesia (RA) covering the previous ten years and concerning autobiographical, semantic and procedural memories. The patient's learning abilities remained excellent and he recovered considerable information from his wife, the media and personal documents. This relearned information did not, however, provide a sense of personal experience in the first weeks. CT and MRI failed to show brain damage, but EEG and SPECT examination showed a marked right temporal dysfunction. After three months the patient had almost completely recovered from RA. Interestingly, a parallel recovery was observed in the second SPECT obtained at this period. There was clearly a blockade of retrieval, while the stored engrams were probably intact. The mechanisms underlying such a functional amnesia are discussed in the light of previous reports of amnesia without brain lesions.

Adult↗

A cholinergic explanation of dense amnesia.

Traditionally, dense amnesia in humans has been thought to be caused by damage to memory structures within the medial temporal lobe, either the hippocampus, the perirhinal cortex or a combination of the two. Recent work in animals has indicated that damage to the hippocampus results in memory impairments that are specific to memories for events. In contrast, damage to the perirhinal cortex impairs object memories in primates, which are likely to be analogous to human semantic memory. Discrete damage to either of these structures does not appear to result in severe and global memory impairments. We propose an alternative to this medial temporal lobe explanation of dense amnesia, based on our recent work. We have shown that the cholinergic cells of the basal forebrain are essential for new learning of both object and event-like memories in the monkey. Our model of learning in the primate brain rests on the proposal that there is a route of communication between the frontal cortex and inferior temporal cortex and hippocampus via the basal forebrain, which is critical for memory encoding. Interruption to this circuit at any stage will result in a severe and global anterograde amnesia.

Amnesia↗

A new case of retrograde amnesia with abnormal forgetting rate.

The classic amnesic syndrome is characterised by a severe anterograde amnesia and a less important retrograde amnesia with sparing of the semantic component. We report the case of a patient who showed a global amnesic syndrome following a mild head injury. Initially, amnesia was both anterograde and retrograde, and also involved semantic knowledge. Two years later the picture had changed remarkably. The retrograde deficit for autobiographical events was still total, while semantic memory had recovered to a large extent. Learning had also greatly improved, but only if assessed after a short delay; abnormally rapid forgetting rate were found at longer intervals. This pattern of impairment does not lend itself to an easy interpretation. However, the hypothesis of a consolidation deficit may be advanced.

Adolescent↗

Persistent retrograde, amnesia following a minor trauma.

A 19-year-old man showed dense retrograde amnesia (RA) for autobiographical and public events covering his entire life, following a motor car accident that caused no apparent brain damage. His learning abilities remained excellent and permitted him to recover knowledge of the past, based on information gathered from other people and the media, although he never reacquired the sense of personal experience. At the onset he also showed occasional gaps in his semantic memory, e.g., he failed to recognize a few objects and was unable to provide factual information about sports he had long been playing. Eventually, his amnesia was predominantly restricted to autobiographical events or facts. After 29 months the deficit has remained unchanged. CT, MRI and PET were negative. Psychogenic amnesia was considered, but eventually ruled out for want of any evidence pointing to emotional problems, stressful situations or secondary gains. We posit that for reasons unknown a mild trauma can cause functional inhibition of the access to the engrams that are already stored, leaving intact the ability to encode and retrieve new memories.

Adult↗

Dual task performance in amnesic and normal people: does resource depletion cause amnesia?

Normal peoples' memory can be seriously disrupted if their cognitive resources are depleted by means of an experimental manipulation (such as distraction at encoding or at retrieval). By analogy, it has also been suggested that amnesia might result directly from pathological loss of cognitive capacity. This hypothesis was examined in 12 mixed amnesics and 12 normal people by means of a 'dual task' study. It was argued that if amnesics have reduced cognitive resources they should be disproportionately impaired in dual task performance relative to single task performance and in comparison to controls. This result was unambiguously demonstrated using a visual (letter detection) task combined with an auditory (semantic decision) task. However, correlations with measures of frontal function and with indicants of severity of amnesia proved insignificant and so the role of resource depletion in amnesia remains, as yet, unproven.

Adult↗

"Psychometric" assessment during transient global amnesia.

A patient "psychometrically" assessed during an attack of transient global amnesia showed total inability to form new long term memories but normal immediate recall. There was nearly perfect preservation of other psychological functions with good recall of distant events and no dysphasia, dyslexia, dysgraphia, dyspraxia, right-left disorientation, constructional apraxia or visual agnosia. Calculation was probably also normal. Some of the 5 previously reported patients, who have been similarly studied during attacks of transient global amnesia, showed evidence of damage to the brain beyond the hippocampal forniceal system. The present patient demonstrates the market selectivity of memory disturbance in "pure transient global amnesia".

Amnesia↗

Transient global amnesia associated with an acute infarction in the retrosplenium of the corpus callosum.

We present a patient with transient global amnesia (TGA) whose diffusion-weighted imaging (DWI) study showed a high-intensity signal in the left retrosplenium of the corpus callosum. In previous studies, lesions in the retrosplenium caused permanent but not transient global amnesia, called retrosplenial amnesia, by involving the thalamocortical portion of the Papez' circuit. This is the first report indicating that TGA can be associated with acute infarction only in the left retrosplenium of the corpus callosum.

Amnesia, Transient Global↗

Right medial thalamic lesion causes isolated retrograde amnesia.

Pervasive retrograde amnesia without anterograde memory impairment has rarely been described as a consequence of circumscribed brain damage. We report this phenomenon in a 33 yr-old, right-handed man (JG) in association with the extension in the right thalamus of a previously small, bilateral thalamic lesion. JG presented with a dense amnesia for autobiographical material more than a few years old, with some sparing of recent memories. Furthermore, he was completely unable to recognise famous people or world events. Many other aspects of semantic knowledge were intact and there was no evidence of general intellectual impairment, executive dysfunction or loss of visual imagery. Magnetic resonance imaging revealed an acute lesion in the right thalamus and two small, symmetrical, bilateral non-acute thalamic lesions. Follow-up neuropsychological assessment indicated a stable pattern of impaired retrograde and spared anterograde memory over 18 months and psychiatric assessments yielded no evidence of confabulation, malingering or other symptoms to suggest psychogenic amnesia. JG's profile indicates that the division of declarative memory into just two categories - episodic and semantic - is inadequate. Rather, his case adds to the growing body evidence to suggest that world knowledge pertaining to people and events is stored or accessed similarly to autobiographical information and differently from other types of more general factual knowledge. We hypothesize that the right mediodorsal thalamic nucleus and immediately surrounding regions comprise the central processing mechanism referred to by McClelland (Revue Neurologique, 150 (1994) 570) and Markowitsch (Brain Research Review, 21 (1995) 117) as responsible for inducing and co-ordinating the recall of these sorts of cortically stored memory engrams.

Adult↗

Acquisition of novel semantic information in amnesia: effects of lesion location.

Two patients with severe global amnesia are described who differ in the extent to which they have acquired new semantic information. Patient SS, who has extensive medial temporal lobe damage including the hippocampus as well as surrounding cortical areas, has failed to acquire virtually any new information regarding vocabulary or famous faces that entered the public domain since the onset of his amnesia. In contrast, patient PS, who has a selective lesion of the hippocampus proper, has gained a sense of familiarity of novel vocabulary and famous people, even though her effortful retrieval of this new semantic knowledge remains impaired. These findings extend to amnesia of adult onset, the proposal of Vargha-Khadem and colleagues that in patients with selective hippocampal injury, cortical areas surrounding the hippocampus may play an important role in new semantic learning [Vargha-Khadem, F., Gadian, D.G., Watkins, K. E., Connelly, A., Van Paesschen, W. and Mishkin, M., regarding the importance of the subhippocampal cortices in the mediation of new semantic learning in children with hippocampal lesions, Science, 1997, 277, 376-380].

Amnesia↗

Does induced recovery from amnesia represent a disinhibition effect?

Induced recovery from amnesia appears similar to disinhibition effects obtained when response strength is weakened in various ways. Therefore, the possibility that reexposure to the amnestic treatment acts as a "disinhibitor" is problematic for a retrieval interpretation of recovery following amnesia. Two experiments examined the question of whether or not hypothermia treatment (i.e., deep body cooling) acts as a disinhibitor for an extinguished fear response in Sprague-Dawley rats. The results of Experiment 1 indicate that deep body cooling did not significantly disinhibit a passive-avoidance response that had previously been extinguished with a 4-min nonreinforced exposure to the shock chamber of the apparatus. Experiment 2 further examined this negative effect by using a modified passive-avoidance procedure and lengthening the extinction session from 4 to 12 min. Similar to Experiment 1, the results of the second experiment also suggested that if the subject's body temperatures were reduced prior to the retention test, no disinhibitory effect of fear conditioning was manifested. These findings support the notion that memory retrieval (i.e., the contextual cue explanation) is the basis for the alleviation of amnesia by reexposure to the amnestic agent.

Amnesia↗

Effects of dynorphin A (1-13) on carbon monoxide-induced delayed amnesia in mice.

The effects of dynorphin A (1-13) on carbon monoxide (CO)-induced amnesia in mice were investigated. Memory deficiency was apparent during Y-maze testing 5 days after CO exposure (delayed amnesia). Percent alternation in the CO-exposed group was significantly lower than that in the control group. Administration of dynorphin A (1-13) (1.5 nmol, i.c.v.) 15 min before the Y-maze test session reversed the impairment of spontaneous alternation performance in the CO-exposed group. To determine whether this effect was mediated via kappa opioid receptors, we attempted to block the effect of dynorphin A using the kappa opioid receptor antagonist nor-binaltorphimine. Nor-binaltorphimine (5.44 nmol, i.c.v.) blocked the effect of dynorphin A (1-13) on delayed amnesia. Dynorphin A (1-13) did not affect the impairment of alternation induced by the blockade of NMDA-receptors by dizocilpine (MK-801), but significantly prevented the impairment induced by mecamylamine. These results suggest that dynorphin A (1-13) modulates the kappa receptor-mediated opioid neuronal system, and reverses the impairment of spontaneous alternation performance induced by CO exposure.

Amnesia↗

Perirhinal cortex lesions produce variable patterns of retrograde amnesia in rats.

Two experiments examined the contribution of the perirhinal cortex (PRh) to retrograde memory for the location of a platform in a water maze. In a previous study, we found that electrolytic lesions of the PRh produced retrograde amnesia, without a temporal gradient, for water-maze problems acquired 4 weeks and 2 days before surgery [Behav. Brain. Res. 114 (2000) 119]. In Experiment 1, we used the same mixed design as in our previous report (time of learning was a within-subjects factor), but PRh lesions were made by aspiration. Contrary to our earlier report, these PRh rats displayed good retention of both platform locations. Combined, these findings indicate that the lesion method may contribute importantly to the pattern of deficits observed. Experiment 2 was conducted similar to Experiment 1, except that a completely between-subjects design was used (time of learning was a between-subjects factor). Rats that received PRh lesions approximately 2 days after the last training session displayed impaired retention of the platform's location, whereas rats that received PRh lesions 4 weeks after training did not. This finding of a temporally graded retrograde amnesia is consistent with our earlier report, and further suggests that the involvement of the PRh in the retention of water-maze problems is time-limited. However, also consistent with our earlier report, the PRh-lesioned rats in Experiment 2 that displayed a retention deficit rapidly reacquired the task. This finding, combined with the negative findings in Experiment 1, suggests that the contribution of the PRh to retrograde memory for platform locations is subtle and may not be due to impaired spatial memory abilities. Additionally, the conflicting results of Experiments 1 and 2 underscore the importance of the design employed in studies of retrograde amnesia in animals.

Amnesia, Retrograde↗

Effects of nefiracetam on amnesia animal models with neuronal dysfunctions.

The effects of N-(2,6-dimethylphenyl)-2-(2-oxo-1-pyrrolidinyl) acetamide (nefiracetam; DM-9384), on learning and memory in several amnesia animal models with neuronal dysfunctions were investigated. Nefiracetam improved scopolamine-, bicuculline-, picrotoxin-, ethanol-, chlordiazepoxide- and cycloheximide-induced amnesia. Anti-amnesic action of nefiracetam on scopolamine model was antagonized by nifedipine and flunarizine, but not by diltiazem. Repeated administration of nefiracetam to AF64A-treated animals improved impairment of learning and memory as well as the alterations in cholinergic and monoaminergic neurotransmitters in the hippocampus. Basal forebrain (BF) lesioned rats induced by excitotoxin or by thermal coagulation showed impairment of learning accompanied by a marked reduction in choline acetyltransferase (ChAT) and acetylcholine esterase activities. Nefiracetam improved the learning deficit of the BF-lesioned rats. Nefiracetam also improved the carbon monoxide-induced delayed and acute amnesia. Nefiracetam stimulated acetylcholine release in the frontal cortex. Repeated administration of nefiracetam increased ChAT activity, gamma-aminobutyric acid (GABA) turnover and glutamic acid decarboxylase activity, and facilitated the Na(+)-dependent high-affinity GABA uptake. Nefiracetam activated the high voltage-activated (N/L-type) Ca2+ channel. The dose-response curves of nefiracetam were bell-shaped in both behavioral and biochemical studies. Therefore, it is suggested that nefiracetam improves the dysfunction of cholinergic, GABAergic and/or monoaminergic neuronal function by acting at Ca2+ channel and enhancing the release of neurotransmitters, and modifies impairment of memory processes induced by drugs and hypoxia.

Amnesia↗