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A model-based study of learning and memory following transient global amnesia attacks.

Verbal learning and forgetting were studied in patients one month after an episode of Transient Global Amnesia and in normal control subjects by means of a two-stage stochastic model, which allows independent measurements of encoding, storage and forgetting. We preliminarily ascertained both the necessity and the sufficiency of the model to account for several performance scores of the two experimental groups, and then compared the learning and forgetting functions between groups. In spite of the analytical power of the statistical method adopted. Transient Global Amnesia was not found to entail persistent impairment of encoding and storage, as well as of retaining memory traces and retrieval algorhythm.

Cerebral Cortex↗

Amnesia is not caused by cognitive slowness.

It has been suggested that the memory disorder in human organic amnesia might be caused by the slow processing of information. Such slowness might be differentially greater for semantic tasks, and/or for tasks requiring the extraction of multiple features of stimuli, or it might simply be a non-specific slowing. These possibilities were tested in a group of alcoholic amnesics and matched normal controls by presenting subjects with a series of words and requiring them to identify one specified word or one of two specified words, or membership of a specified category or one of two specified categories. Although amnesics' reaction times were slightly slower than controls' the effect was insignificant, and there was no hint of differential slowing in the semantic or multiple processing tasks. It was concluded from these results and a consideration of the reaction time literature that cognitive slowness is unrelated to the main cause of amnesia.

Alcohol Amnestic Disorder↗

Word priming with brief multiple presentation technique: preservation in amnesia.

Many studies have shown relative preservation of word priming in subjects with mild amnesia, but some decrease in severe amnesia. This calls into question the degree of separation between implicit and explicit memory. Possible contamination of implicit memory tasks by impaired explicit memory strategies might be obscuring the actual dissociation between the two memory systems. We have developed a method of circumventing explicit memory contamination by using brief duration repeated primes below the awareness threshold of subjects. We have used this approach to evaluate the status of word priming in densely amnesic subjects. One group of amnesic subjects with alcoholic Korsakoff's syndrome and one group of normal elderly control subjects were tested for word priming on a speeded category membership decision task. Implicit or explicit encoding procedures were used in three different experiments. Results demonstrated that brief multiple presentation of words can offer a means of producing word priming in the absence of explicit recognition or recall of the primed words in both amnesic subjects and normal elderly control subjects. Moreover, there was no significant difference in the magnitude of the priming effect between these groups in the three experiments. These findings show that amnesic subjects can exhibit normal levels of word priming. They also suggest that amnesics retain the capacity to encode, store and retrieve information implicity, e.g. unintentionally.

Aged↗

Post-training intrahippocampal infusion of protein kinase C inhibitors causes amnesia in rats.

This experiment investigated the effect on memory, in rats, of the bilateral intrahippocampal post-training infusion of two different inhibitors of protein kinase C activity, staurosporin and CGP41231. Male Wistar rats were implanted bilaterally with cannulae aimed at the CA1 region of the dorsal hippocampus. After recovery from surgery, they were trained in step-down inhibitory avoidance using a 0.5-mA footshock and tested for retention 24 h later. Immediately or 30, 120, or 180 min after training they received, through the cannulae, infusions of vehicle, staurosporin (1.0 microgram), or CGP41231 (2.5 micrograms). The two drugs caused full retrograde amnesia when given immediately or 30 min post-training, partial amnesia when given 120 min after training, and had no effect when given 180 min after training. The results support the suggestion that memory involves long-term potentiation initiated at the time of training in the hippocampus. Inhibitors of protein kinase C block the development of long-term potentiation when administered in the first 2 h after induction.

Alkaloids↗

Scopolamine amnesia of passive avoidance: a deficit of information acquisition.

Despite its increasing use as an animal model of memory deficit in human dementia, relatively few studies have attempted to assess the memory processes involved in the anticholinergic-induced impairment of passive avoidance retention. In the present experiments, the influence of scopolamine administered prior to or immediately following training on 24-h retention of step-through passive avoidance was studied in NMRI mice. In low doses (0.3-3.0 mg/kg ip) pretraining administration (-5 min) of scopolamine induced a very strong amnesia. Post-training scopolamine induced a significant effect only at the highest dose tested (30 mg/kg). In a retention test of longer than normal duration (600 vs 180 s), which resulted in a more favorable comparison value in the control group, an intermediate post-training dose (10 mg/kg) induced a small effect which approached significance; a finding which may account for conflicting reports in the literature concerning the ability of scopolamine to induce a post-training deficit. The pretraining effect does not appear to have been solely the result of state-dependent learning; scopolamine (3 mg/kg) administered before both the training and test sessions induced a deficit of approximately the same magnitude as that found when administered before training or before testing only. The results indicate that scopolamine can induce a small post-trial effect, presumably through an influence on consolidation processes. The much larger effect of pretrial scopolamine, however, indicates a primary influence on processes related to information acquisition. Together with findings from the literature, the present experiments suggest that scopolamine-induced amnesia partially, but not completely, models the memory deficits of human dementia.

Animals↗

The ventral hippocampus and fear conditioning in rats: different anterograde amnesias of fear after infusion of N-methyl-D-aspartate or its noncompetitive antagonist MK-801 into the ventral hippocampus.

Previous studies on hippocampal involvement in classical fear conditioning mainly focused on the dorsal hippocampus and conditioning to a context. However, in line with the strong interconnectivity of the ventral hippocampus with amygdala and nucleus accumbens, more recent studies indicated an even more global role for the ventral hippocampus in fear conditioning. The present study examined the formation of classical fear conditioning to explicit and contextual cues following stimulation or blockade of N-methyl-D-aspartate (NMDA) receptors in the ventral hippocampus. NMDA (0.5 microg/side) or the noncompetitive NMDA antagonist MK-801 (dizocilpine; 6.25 microg/side) were bilaterally infused into the ventral hippocampus of Wistar rats before fear conditioning to explicit and contextual cues. Conditioned fear was assessed using an automated measurement of freezing. NMDA stimulation of the ventral hippocampus blocked fear conditioning to both the tone and the context. MK-801 selectively blocked fear conditioning to the context. Our results support that the ventral hippocampus plays a role in the formation of classical fear conditioning. The specific anterograde amnesia for fear to a context after MK-801 infusion into the ventral hippocampus indicates that formation of classical fear conditioning to a context but not to a tone requires activation of NMDA receptor-mediated processes in the ventral hippocampus. Given that NMDA stimulation of the ventral hippocampus disrupts also processes not mediated by NMDA receptors, the complete anterograde amnesia following NMDA infusion into the ventral hippocampus might be due to the concurrent severe disruption of normal ventral hippocampal activity. However, strong stimulation of the ventral hippocampus might also disrupt fear conditioning by interfering with processes in the projection areas of the ventral hippocampus, such as the amygdala or the nucleus accumbens. In addition, we report that MK-801 (6.25 microg/side) infusion into the ventral hippocampus increased locomotor activity in the open field.

Amygdala↗

Vasopressin and memory: improvement in normal short-term recall and reduction of alcohol-induced amnesia.

The 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.

Adult↗

Severe global amnesia presenting as Wernicke-Korsakoff syndrome but resulting from atypical lesions.

A female alcoholic presented with Wernicke's encephalopathy subsequent to administration of diazepam and glucose (without thiamine) for treatment of withdrawal seizures. Nystagmus and cerebellar ataxia quickly resolved when administered thiamine, although severe global amnesia consistent with Korsakoff's syndrome persisted. Magnetic resonance imaging (MRI) revealed infarction of the right temporal lobe with hippocampal atrophy, but no lesions of thalamus or atrophy of mammillary bodies. Positron emission tomography (PET) confirmed decreased cerebral metabolic rates for glucose (CMRglu) in the right temporal lobe corresponding to MRI findings, but also significant metabolic asymmetry of dorsal thalamus, i.e. reduced CMRglu in left versus right. This patient is unique in that neuroradiological findings revealed intact mammillary bodies and suggest asymmetrical dysfunctions (structural right temporal and functional left diencephalic) to produce her profound amnesia.

Alcohol Amnestic Disorder↗

Paired-associate learning and priming effects in amnesia: a neuropsychological study.

Despite severe deficits of recall and recognition, amnesic patients can exhibit normal priming effects. Amnesic patients have also been reported to perform well on tests of paired-associate learning that involve related word pairs (e.g., table-chair). The present study investigated the role of priming effects in paired-associate learning. Experiment 1 illustrated the distinction between the memory impairment of amnesic patients and their intact priming ability. Amnesic patients were markedly deficient in learning unrelated word pairs, despite exhibiting normal priming as measured by a word-completion test involving the same words. In Experiment 2A, amnesic patients showed good paired-associate learning for related word pairs, though control subjects still performed significantly better. In addition, the good performance by amnesic patients was short-lived, and performance fell to baseline after a 2-hr delay. Control subjects performed well above baseline at all delay conditions. Experiment 2B showed that the forgetting of related word pairs by amnesic patients followed the same time course as the decay of word priming. Experiment 3 showed that amnesic patients were as good as control subjects at learning related word pairs when incidental learning and test procedures were used (a word-association test). The advantage of control subjects over amnesic patients in Experiments 2A and 2B could therefore be attributed to the explicit learning instructions that are standard in paired-associate tests. Finally, Experiment 4 showed that amnesic patients exhibited normal priming when they were asked to "free associate" to words (e.g., child) that were semantically related to previously presented words (e.g., baby). The results indicate that both priming effects and paired-associate learning of related word pairs depend on activation, a process that is preserved in amnesia. Activation can account for the findings of good performance by amnesic patients on tests of word priming (Experiments 1 and 2B), related paired associates (Experiments 2A and 2B), and word association (Experiments 3 and 4). Activation is a transient phenomenon presumed to operate on and facilitate access to preexisting representations. Control subjects can establish new associations and can strengthen preexisting associations by engaging processes that are impaired in amnesia. As a result, when explicit learning instructions are used to test paired-associate learning of related word pairs, control subjects can learn better and can remember longer than can amnesic patients (Experiments 2A and 2B).(ABSTRACT TRUNCATED AT 400 WORDS)

Alcohol Amnestic Disorder↗

Lack of a temporal gradient of retrograde amnesia in rats with amygdala lesions assessed with the fear-potentiated startle paradigm.

It is well known that lesions of the hippocampal formation produce a temporally graded retrograde amnesia for certain types of memory. A similar pattern of results has been reported with amygdaloid lesions in avoidance learning (K.C. Liang et al., 1982). The present study examined the effects of posttraining amygdaloid lesions using a Pavlovian conditioning task, fear-potentiated startle, in which the amplitude of the acoustic startle reflex is increased when elicited in the presence of a cue (e.g., a light) previously paired with footshock. Electrolytic lesions of the amygdala given either 6 or 30 days after training blocked the expression of potentiated startle, indicating no temporal gradient of amnesia over these intervals in this paradigm. The effects of amygdaloid lesions on different measures of aversive learning are discussed.

Amygdala↗

A randomized, double-blind, placebo-controlled study of methylphenidate in patients with organic amnesia.

We examined the usefulness of methylphenidate (MPH) in the treatment of organic amnesia in a randomized, double-blind, placebo-controlled design. Twenty patients with amnesia due to closed head injuries (n = 10), viral encephalitis (n = 2), stroke lesions (n = 4), or surgical brain resections (n = 4) were assessed with a neuropsychological battery after the intake of MPH (10, 20, 30 or 40 mg), or placebo. We found no significant benefit of MPH for any of the cognitive tests.Copyright Lippincott-Raven Publishers

Journal Article↗

Nonverbal signs of deception during posthypnotic amnesia: a brief communication.

The question of hypnotic subjects complying with instructions, perhaps even purposely deceiving the hypnotist or deceiving themselves, has arisen from the state-nonstate (skeptical-credulous) theoretical controversy. However, experimental testing of competing hypotheses has been difficult. The current report offers methodological procedures that may prove useful. Subjects who were given posthypnotic amnesia instructions were tested on free recall and implicit recall of a 20-word list. To detect the possibility of deception, videotapes of real subjects and simulating subjects during and after posthypnotic amnesia were rated for nonverbal signs of deception, signs taken from the works of Ekman, Ekman and Friesen, and Zuckerman et al. Preliminary results were gathered on a small pilot sample, and recommendations for procedural improvements are proposed.

Awareness↗

Attention-related electroencephalographic and event-related potential predictors of responsiveness to suggested posthypnotic amnesia.

Higher frequency electroencephalographic (EEG) activity around 40 Hz has been shown to play a role in cognitive functions such as attention. Furthermore, event-related brain potential (ERP) components such as N1 and P1 are sensitive to selective attention. In the present study, 40-Hz EEG measures and early ERP components were employed to relate selective attention to hypnotic response. Participants were 20 low hypnotizable individuals, half assigned as simulators, and 21 high hypnotizable individuals. Each of these groups was subsequently divided into two groups based on recognition amnesia scores. The four groups differed in 40-Hz (36-44 Hz) EEG spectral amplitude recorded during preinduction resting conditions but not in EEG amplitude postinduction. The groups also differed in N1 amplitudes recorded during hypnosis. Regression analysis revealed that these effects only distinguish the high hypnotizable participants who experienced recognition amnesia from all other groups. The findings support the role of selective attention in hypnotic responsiveness, and the utility of subdividing high hypnotizable individuals is discussed.

Adolescent↗

Hypnotizability, the dissociative experiences scale, HGSHS: A amnesia, and automatic writing: is there an association?

The present study examined whether participants (N = 112) selected on the basis of high and low dissociative ability (Dissociative Experiences Scale [DES]; Bernstein & Putnam, 1986), high and low/simulating hypnotizability (Harvard Group Scale of Hypnotic Susceptibility, Form A [HGSHS:A]; Shor & Orne, 1962), and past performance on the HGSHS:A amnesia item differentially passed an automatic writing suggestion administered during a follow-up experiment. Results from a loglinear analysis supported a single main effect for hypnotizability. Low hypnotizable, simulating participants were more than six times as likely to pass the automatic writing suggestion than high hypnotizable participants. Results found dissociation status and past performance on an ostensibly dissociative suggestion (i.e., amnesia) to be independent of passing the automatic writing suggestion. Findings are discussed in light of other research regarding the relation between the DES and hypnotizability.

Adult↗

Memory function after resolution of post-traumatic amnesia.

PRIMARY OBJECTIVES: The aims of this pilot study were (1) to examine neuropsychological, particularly memory functions immediately after post-traumatic amnesia (PTA) resolution according to the Galveston Orientation and Amnesia Test (GOAT), and (2) to provide a preliminary exploration of pattern of performance on GOAT items across PTA duration. METHODS AND PROCEDURES: Thirty-seven head injured patients were administered the Recognition Memory Tests on the day that PTA resolved. Formal neuropsychological assessment was conducted on average 10 days after PTA resolution. MAIN OUTCOMES AND RESULTS: All the patients in the series showed memory impairment which varied in severity but was typically characterized as global and severe. Deficits in executive and speed and attention functions were common. GOAT items relating to orientation were typically passed, while items concerning anterograde and retrograde recall were most commonly failed across all stages of PTA duration. CONCLUSIONS: These findings suggest that reliance on memory performance as a measure of PTA is not ideal and highlight the need for further research of this issue.

Adult↗

No selective deficit in recall in amnesia.

Are amnesic patients selectively impaired in recall relative to recognition? Experiment 1 studied a group of Korsakoff amnesics and matched the amnesic level of recognition with that of control subjects by testing control recognition of unrelated words after longer delays. It was found that under these conditions the observed levels of recall were also approximately equal. In Experiment 2, a similar result occurred when the Korsakoff amnesic level of recognition for unrelated words was matched by varying the number of presentations as well as delay before testing. In Experiment 3, a similar result occurred again with a group of amnesics of mixed aetiology and recognition levels for related words matched by varying the duration of presentation and delay before testing. In this experiment, both recognition and recall of the same items were assessed. It was found that for the amnesic group the observed level of dependency between recognition and recall was less than that for the control group. One possible interpretation of this result is that the microstructure of the recall process may be selectively disturbed in amnesia. The principal finding, however, is that in all three experiments there was no significant evidence of the existence in amnesia of a selective deficit in the overall level of recall relative to that of recognition.

Adult↗

Assumptions of infantile amnesia: are there differences between early and later memories?

Most adults are able to provide few, if any, reports of autobiographical memories from the first years of life. Early memories that do exist have been characterised as highly emotional, containing an abundance of perceptual as opposed to propositional information, and more often in the third than the first person perspective. These qualities figure prominently in theories of the source of the phenomenon of infantile amnesia. However, early and later memories have not been directly compared with regard to these features. In the present research, we compared early and later memories in the same individuals, with the same methodology. Results indicated few objective differences between the early and later memories of women (Experiment 1) and men (Experiment 2). The findings are discussed in light of their implications for theories as to the source of infantile amnesia.

Adult↗

Can PTSD Occur with Amnesia for the Precipitating Event?

Theoretical accounts of post-traumatic stress disorder (PTSD) suggest that memory for a precipitating event is crucial for its development. Indeed, Sbordone and Liter (1995) have recently argued that mild traumatic brain injury and PTSD are mutually exclusive disorders. A case is described who sustained a severe head injury in a road traffic accident. He had a retrograde amnesia of two days and a post-traumatic amnesia of four weeks. Six months after his accident he was found to be suffering from a number of anxiety symptoms, including nightmares and intrusive thoughts, consistent with a diagnosis of PTSD. The implications of this case for theories of PTSD are discussed.

Journal Article↗