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PubMed2000

"Amnesia" for summer camps and high school graduation: memory work increases reports of prior periods of remembering less.

Claims regarding amnesia for childhood sexual abuse have often been based on studies of adults' responses to questions of the form, "Was there ever a period of time when you remembered less of the abuse than you do now?" In this experiment, 43 adult (mean age = 42) participants rated their current and prior memories of several nontraumatic childhood/adolescent events. Reports of prior periods of less memory were fairly common. Participants then engaged in "reminiscence" or "enhanced" retrieval activities directed toward remembering more about a selected target event. Following retrieval, 35% of the reminiscence condition participants reported prior poor memory for the target event, as did 70% of the enhanced condition. These results highlight the need for appropriate control conditions in retrospective studies of amnesia for childhood trauma.

Adolescent↗
PubMed1998

Traumatic amnesia, repression, and hippocampus injury due to emotional stress, corticosteroids and enkephalins.

The role of stress, arousal, emotional trauma, and corticosteroid and enkephalin secretion on memory and the hippocampus, and the development of traumatic amnesia and repressed memory syndrome are detailed. Animal and human studies are reviewed. Trauma-induced memory deficits appear to be secondary to abnormal neocortical and hippocampal arousal, and corticosteroid and enkephalin secretion which can induce atrophy or seizures within the hippocampus, suppress hippocampal theta activity and long term potentiation, as well as injure hippocampal pyramidal cells. Predisposing factors include individual, age, and sex differences in arousal, and previous emotional trauma or temporal lobe or hippocampal injury. However, as the amygdala processes and stores emotional experiences in memory, patients may also demonstrate trauma related symptoms, including flashbacks as well as shrinking retrograde amnesia.

Adrenal Cortex Hormones↗
PubMed2003

Status of the "protein kinase CK2-HMG14" system in age-related amnesia in rats.

The experiments described here demonstrate that disruption of the phosphorylation of transcription factors of the HMG cAMP/Ca-independent protein kinase CK2 class may be the cause of decreased gene expression in age-related cognitive deficits. Amnesia for a conditioned passive avoidance reaction (CPAR) in aged rats (24 months old) was accompanied by decreases in the synthesis of synaptosomal proteins and transcription in nuclei isolated from cortical, hippocampal, and striatal neurons. There was a decrease in chromatin protein kinase CK2 activity and a significant decrease in the phosphorylation of HMG14 by protein kinase CK2. Selective activators of protein kinase CK2 (1-ethyl-4-carbamoyl-5-methylcarbamoylimidazole and 1-ethyl-4,5-dicarbamoylimidazole) increased HMG14 phosphorylation by protein kinase CK2, increased transcription, increased the synthesis of synaptosomal proteins, and decreased amnesia for the CPAR in aged rats. Thus, activation of the "protein kinase CK2-HMG14" system is accompanied by optimization of synaptic plasticity in aged animals. The results provide evidence for the high therapeutic potential of protein kinase CK2 activators.

Aging↗
PubMed2000

Transient global amnesia: a review emphasizing pathogenic aspects.

The transitory memory disturbance known as transient global amnesia (TGA) remains an enigma from a pathogenic point of view. In spite of its typical benign prognosis, TGA is a frightening experience for patients and their relatives. Moreover, a TGA episode usually leads to extensive investigation of patients in search of organic alterations that might be responsible for the event. Finally, TGA generates queries about therapeutic choices. In this review, we critically re-evaluate the evidence in support of and against the three main pathogenic hypotheses (i.e. ischemia, seizure discharge, and migraine), and we conclude that none of these appears completely convincing. Given the good prognosis and the lack of association with organic and instrumental abnormalities, we advance the hypothesis that TGA may be related to psychological disturbances causing transient alteration in brain metabolism and, consequently, amnesia. Our conclusion has relevant consequences in the evaluation of patients with TGA.

Age Factors↗
PubMed2001

Journey to the center of the category: the dissociation in amnesia between categorization and recognition.

The authors' theoretical analysis of the dissociation in amnesia between categorization and recognition suggests these conclusions: (a) Comparing to-be-categorized items to a category center or prototype produces strong prototype advantages and steep typicality gradients, whereas comparing to-be-categorized items to the training exemplars that surround the prototype produces weak prototype advantages and flat typicality gradients; (b) participants often show the former pattern, suggesting their use of prototypes; (c) exemplar models account poorly for these categorization data, but prototype models account well for them; and (d) the recognition data suggest that controls use a single-comparison exemplar-memorization process more powerfully than amnesics. By pairing categorization based in prototypes with recognition based in exemplar memorization, the authors support and extend other recent accounts of cognitive performance that intermix prototypes and exemplars, and the authors reinforce traditional interpretations of the categorization-recognition dissociation in amnesia.

Amnesia↗
PubMed1997

Impaired trace eyeblink conditioning in bilateral, medial-temporal lobe amnesia.

Trace eyeblink classical conditioning was assessed in patients with bilateral medial-temporal amnesia and matched control participants who had previously shown equivalent delay eyeblink conditioning (J. D. E. Gabrieli et al., 1995). The silent trace interval varied for durations of 500, 750, or 1,000 ms in successive sessions separated by at least 2 weeks; extinction trials followed each session. Patients with amnesia produced significantly fewer conditioned responses (CRs) than did control participants at all trace intervals. Both groups produced fewer CRs as the trace interval lengthened. Thus, the temporal lobe memory system in humans makes an essential contribution to normal acquisition in trace, but not delay, classical eyeblink conditioning.

Adult↗
PubMed1985

Medial temporal lesions in monkeys impair memory on a variety of tasks sensitive to human amnesia.

Monkeys with conjoint bilateral lesions of the hippocampus and amygdala were impaired on four different tests of memory (delayed retention of object discriminations, concurrent discrimination, delayed response, and delayed nonmatching to sample). Because tests involving delays and distractions are known to be especially sensitive to human amnesia, in three of the tasks relatively long delay intervals between training and test trials were used, and in two tasks distraction was introduced during the delay intervals. The severity of the impairment increased with the length of the delay, and distraction markedly increased the memory impairment. For one task given on two occasions (delayed nonmatching to sample), the severity of the impairment was unchanged over a period of 1.5 years. Taken together with previous findings that skill learning is unimpaired in the same operated monkeys, the results of the present study strengthen the conclusion that monkeys with medial temporal lesions constitute an animal model of human amnesia. In addition, the four tasks used here appear to constitute a sensitive and appropriate battery that could be used in other studies of the neuroanatomy of memory functions in the monkey.

Amnesia↗
PubMed1997

Emotional perception and memory in amnesia.

The authors examined whether perception of emotional stimuli is normal in amnesia and whether emotional arousal has the same enhancing effect on memory in amnesic patients as it has in healthy controls. Forty standardized color pictures were presented while participants rated each picture according to emotional intensity (arousal) and pleasantness (valence). An immediate free-recall test was given for the pictures, followed by a yes-no recognition test. Arousal and valence ratings were highly similar among the amnesic patients and controls. Emotional arousal (regardless of valence) enhanced both recall and recognition of the pictures, and this enhancement was proportional for amnesic patients and controls. Results suggest that emotional perception and the enhancing effect of emotional arousal on memory are intact in amnesia.

Aged↗
PubMed1997

Persistent global amnesia following right thalamic stroke: an 11-year longitudinal study.

The 11-year longitudinal study of a right-handed male patient, L. C., who suffered from a severe amnesic syndrome following a softening in the right thalamus, is reported. Memory impairment involving retrograde and long-term anterograde memory, both verbal and spatial, persisted without modification. Investigation revealed some residual implicit learning ability. Positron emission tomography studies in the resting state displayed a bilateral hypometabolism of the mesial frontal lobes. Evidence suggests that a lesion confined to the thalamus may not on its own account for severe amnesia; that involvement of other structures is necessary for severe amnesia to appear; and that a functional investigation should always be included in cases of small thalamic lesions before drawing conclusions about the structures responsible for a given deficit.

Aged↗
PubMed2006

Benjamin Franklin and shock-induced amnesia.

Shock-induced amnesia received considerable attention after Cerletti popularized electroconvulsive shock therapy in the late 1930s. Yet, often overlooked is the fact that Benjamin Franklin recognized that passing electricity through the head could affect memory for the traumatic event. Franklin described his findings on himself and others in several letters from the mid-1700s, 2 of which were published in his lifetime. What he observed was confirmed in 1783 by physician Jan Ingenhousz, who was one of his correspondents. Although Ingenhousz had lost his memory for his electrical accident and was confused immediately afterward, he felt strangely elated and unusually sharp the next morning. Hence, he called for clinical trials with patients with melancholia who were not responding to more conventional therapies. After Franklin received Ingenhousz's letter, he also called for clinical trials. Neither man, however, tied the possible new cure for melancholia to the memory loss--nor did the operators that began to treat some patients with melancholia successfully with cranial shocks. Only much later would the amnesia be thought to be associated with the cure.

Amnesia↗
PubMed1993

Drug-induced amnesia: implications for cognitive neuropsychological investigations of memory.

Studies of drug effects on memory represent a large body of literature that, for the most part, has not had an impact on psychological theories of memory and amnesia produced by cognitive psychologists, who tend to theorize independently of information about the brain. Recently, however, there has been a movement toward cognitive neuropsychological approaches to memory in which theorists have begun to consider, and even focus on, neuroanatomical realities. This approach currently relies on data from organic amnesic patients and normal Ss. This article suggests that studies of drug-induced amnesia complement these current lines of investigation and therefore merit consideration from cognitive neuropsychologists interested in memory. To this end, the drugs and memory literature is reviewed, and its potential relationship with more mainstream cognitive neuropsychology is discussed.

Amnesia↗
PubMed2003

Temporally graded, context-specific retrograde amnesia and its alleviation by context preexposure: effects of postconditioning exposures to morphine in the rat.

Five experiments studied retrograde impairments in Pavlovian fear conditioning following prolonged exposure to the opioid receptor agonist morphine. Injections of morphine commencing 1-7 days but not 14 days after conditioning produced amnesia for that conditioning episode. This amnesia was (a) selective such that morphine impaired freezing to the conditioning context but not to the auditory conditioned stimulus, (b) independent of the interval between the last injection of morphine and test, and (c) accompanied by a failure of contextual discrimination. Context preexposure protected context conditioning and discrimination from the amnestic effects of morphine. These results show that retrograde deficits in contextual fear conditioning are mediated by failures to consolidate a contextual representation.

Acoustic Stimulation↗
PubMed2004

Retrograde amnesia induced by drugs acting on different molecular systems.

The gamma aminobutyric acid-A (GABA-sub(A)) agonist, muscimol, the glutamate N-methyl-D-aspartate (NMDA) receptor antagonist, D-2-amino-5-phosphonopentanoic acid (AP5), and the inhibitor of the extracellularly regulated kinases (ERKs), UO 126, cause retrograde amnesia when administered to the hippocampus. In the present study, the authors found that they all cause retrograde amnesia for 1-trial inhibitory avoidance, not only when infused into the dorsal CA1 region of the hippocampus, but also when infused into the basolateral amygdala or the entorhinal, parietal, and posterior cingulate cortices. The posttraining time course of the effect of each drug was, however, quite different across brain structures. Thus, in all of them, NMDA receptors and the ERK pathway are indispensable for memory consolidation, and GABA-sub(A) receptor activation inhibits memory consolidation: but in each case, their influence is interwoven differently.

Amnesia, Retrograde↗
PubMed2006

Recovery of fear memories in rats: role of gamma-amino butyric acid (GABA) in infantile amnesia.

Infantile amnesia is a ubiquitous phenomenon, but its neural bases remain largely unknown. The authors identify a role for GABAergic transmission in suppressing retrieval of memories acquired in infancy. Eighteen-day-old rats received pairings of white noise and shock; considerable forgetting of this experience (assessed by freezing) occurred after 10 days. The memory was recovered by pretest administration of the GABAA inverse agonist FG7142 10 days, but not 2 months, after training. This effect of FG7142 generalized when a passive avoidance procedure was used. Also, FG7142 decreased fear of a latently inhibited conditioned stimulus, showing that the observed memory recovery effect was not due to a state-dependent process. It appears that GABA may be involved in infantile amnesia regardless of the emotional content of the memory.

Amnesia↗
PubMed2006

Increased interhemispheric interaction is associated with earlier offset of childhood amnesia.

Experiment 1 found that mixed-handedness, which is associated with increased interaction between the left and right cerebral hemispheres relative to strong right-handedness, was associated with an earlier offset of childhood amnesia. In Experiment 2, bilateral saccadic eye movements, which have been shown to enhance interhemispheric interaction, were also associated with an earlier offset of childhood amnesia. These results build upon a growing body of research indicating an interhemispheric basis for the retrieval of episodic memories. Moreover, the results of Experiment 2 suggest that interhemispheric interaction has its effect on the retrieval, not encoding, of episodic memories.

Adolescent↗
PubMed1975

Factors in the modification by isolation of electroconvulsive shock-produced retrograde amnesia in the rat.

It has been demonstrated that placing rats in a sensory-restricted environment during the electronconvulsive shock- (ECS) retention interval following 1-trial appetitive learning will prevent or eliminate ECS-produced retrograde amnesia. The first study replicated this finding with a 1-trial aversive learning task, indicating that this effect is not task specific. The second study attempted to determine whether illumination or the restricted environment was the crucial factor in this penomenon. Rats placed in the light during the ECS-retention interval, whether restricted or in the colony, demonstrated retrograde amnesia after ECS. However, rats left in the dark during this interval demonstrated little, if any, retention deficit particularly if this condition was combined with sensory isolation. These studies further indicate that manipulation of the general environment of the animal after ECS can alter ECS-produced retention losses.

Amnesia↗
PubMed2005

Disruption of sequential priming in organic and pharmacological amnesia: a role for the medial temporal lobes in implicit contextual learning.

We examined learning and expression of contextual implicit learning of a sequence of targets in a speeded target-detection task in amnesic and control participants. Amnesia was of organic origin in one participant group and induced psychopharmacologically (diazepam 7.5 or 15 mg) in another. Although the amnesic groups were able to learn the target sequence normally, their expression of sequence knowledge (priming) was attenuated when contextual support was limited. This was evaluated by studying response latencies for targets primed by between 0 and 5 preceding context locations. Whereas control participants showed priming when the current target location was primed by only two previous locations, priming was eliminated with two (but not four) previous locations by a low dose of diazepam and was eliminated even with four elements of context under a high dose of diazepam and in amnesia of organic origin. The results suggest that a function of the hippocampal memory system is to support contextual learning and performance, even when that learning is nondeclarative.

Adolescent↗
PubMed1998

Retrograde amnesia for spatial information: a dissociation between intra and extramaze cues following hippocampus lesions in rats.

Several recent studies have shown a flat retrograde amnesia for spatial information following lesions to the hippocampus in rats and mice. However, the results of the present investigation demonstrate that in rats that presurgically learned a spatial reference memory task based on extramaze cues, a temporally graded retrograde amnesia is evident following lesions to the hippocampus (1, 16, 32 or 64 days after learning) if two conditions are met. First, that a wide range of retention intervals is used, and second, that independent groups of rats are tested, not a single group that learns different spatial discrimination tasks at different times (expt 1). The results of expt 2 show that the hippocampus does not serve as a consolidating mechanism when the spatial task learned presurgically is based on intramaze cues. Taken together, these results indicate that the hippocampus is critical for the storage and/or retrieval of spatial reference information that was learned up to 1 month before hippocampus damage; however, in the absence of the hippocampus, efficient retention can still occur provided that the spatial knowledge was learned in a simple associative manner.

Amnesia, Retrograde↗