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PubMed1996

Hypnotic amnesia and the paradox of intentional forgetting.

Hypnotic amnesia is often interpreted as a deliberate effort to avoid thinking of ideas or thoughts targeted for amnesia. However, as D.M. Wegner (1989) showed, nonhypnotized individuals who deliberately attempt to suppress certain thoughts or images paradoxically suffer intrusions of the prescribed material. The authors replicated Wegner's findings in 2 separate investigations. However, they also found that hypnotic amnesia did not have such paradoxical effects. Indeed, the great majority of high-hypnotizable individuals administered suggestions for amnesia showed no such intrusions whatsoever, indicating that thought suppression and hypnotic amnesia represent quite different processes.

Adult↗
PubMed1989

Preventing and alleviating hypothermia-induced amnesia in weanling and young adult rats.

Reminder (Experiment 1) and familiarization (Experiment 2) treatments were found to have similar effects on the 24-hr retention performance of 24- to 26- and 90- to 100-day-old rats that either did or did not undergo an amnesic treatment (hypothermia) immediately after training. Similar degrees of retrograde amnesia and normal forgetting were evident in both trained age groups that were not subjected to familiarization or reminder treatments. These results suggest that memory processes in weanling and adult rats are similar in susceptibility to disruption by an established amnesic treatment (hypothermia) and in the ease of prevention of and recovery from amnesia by recognized preventive (familiarization) and alleviation (reminder) measures. The similarity of the effects of these preventive and alleviation treatments on normal forgetting and induced amnesia suggests that experimentally induced amnesia may be a fruitful approach to studying the ontogeny of memory processes and, more specifically, to studying factors that influence infantile amnesia.

Aging↗
PubMed1998

Questionable validity of 'dissociative amnesia' in trauma victims. Evidence from prospective studies.

BACKGROUND: We reviewed evidence from prospective studies to test whether individuals can develop amnesia for traumatic experiences, a process variously termed 'repression', 'dissociative amnesia' or 'psychogenic amnesia'. METHOD: Using specified criteria, we selected and analysed studies which prospectively assessed memory in victims of documented traumatic experiences. RESULTS: In studies in which people were asked directly about a past traumatic experience, they consistently reported memories. Non-reporting occurred only in studies where subjects were not asked directly about the experience. This latter design leaves open the well-documented possibility that subjects simply did not disclose events that they actually remembered. Some prospective studies were also limited by incomplete documentation of trauma and failure to rule out other more ordinary causes of amnesia. CONCLUSIONS: Prospective data as yet fail to demonstrate that individuals can develop dissociative amnesia for traumatic events.

Adult↗
PubMed2000

Functional neuroanatomy of amnesia: positron emission tomography studies.

In this article, we review the principles of, and provide examples for, the new approach of functional neuropsychology in the field of amnesia. In the permanent amnesic syndrome, positron emission tomography (PET) can provide statistical maps of the brain regions with significantly impaired resting metabolism in comparison with control subjects. These regions include not only Papez's circuit but also the left supramarginal gyrus, which may explain in part the retrograde amnesia present in most cases of amnesic syndrome. This approach is also of great interest in transient global amnesia (TGA) because the defect of episodic memory is highly selective and occurs without permanent damage. The few available PET studies in TGA suggest the dysfunction of a distributed network including the hippocampal region and the prefrontal cortex, with a different pattern individually. Further studies will be necessary to better understand the relationships between the precise cognitive deficits in TGA and the pattern of brain hypometabolism. In Alzheimer's disease (AD), the study of the correlations between memory test scores and metabolic values across a sample of subjects provides a map of those brain structures whose synaptic pathology dysfunction underlies the particular neuropsychological alteration. The distribution of the sites of correlations shows striking differences according to each memory system. This approach should open the way for the unravelling of the neurobiological substrates of both cognitive impairment and compensatory mechanisms in neurodegenerative diseases. Over and above their applications in neurological research, such studies in brain-diseased subjects are particularly useful for establishing cognitive and neurobiological models of human memory, because they allow the highlighting of the neural networks that are essential for memory function. From a cognitive neuroscience perspective, the functional neuropsychology of amnesia is, therefore, complementary to the classic activation paradigm in normal subjects, which identifies the cerebral structures that are involved with, but not necessarily indispensable for, the execution of the task.

Alzheimer Disease↗
PubMed1982

Nonmonotonic age changes in susceptibility to hypothermia-induced retrograde amnesia in rats.

The effects of post-training and/or pretesting body cooling on retention of Pavlovian discriminated fear conditioning were examined in preweanling (16-day) and weanling (23-day) rats. Twenty-four retention was assessed in 16- and 23-day-old rats receiving hypothermia after training, after training and prior to testing, or at neither time. Amnesia was present in the preweanling but not weanling rats. Recovery from amnesia was not observed in the preweanling rats followed a second cooling treatment. Control groups indicated the differential amnesia was not the result of differences in 24 hr baseline retention, depth of hypothermia cooling, rate of recovery from hypothermia treatment, or body temperature immediately post-testing. The results are discussed with respect to current views of infantile amnesia and the growing evidence for similar nonmonotonic functions during ontogeny.

Age Factors↗
PubMed1985

Disrupting circadian rhythms in rats induces retrograde amnesia.

Disrupting circadian organization in rats by phase-shifting the illumination cycle or by exposure to a reversed day/night cycle or to continuous light, resulted in retrograde amnesia for passive avoidance behavior. This retrograde amnesia induced by phase-shifting lasted at least 2 days, and gradually diminished the longer the rats were exposed to the new illumination cycle. Retention performance was not impaired when rats were exposed to phase-shifting for 3-5 days before the learning trial. The retrograde amnesia due to changing the illumination cycle is probably due to retrieval disturbances. Extinction of active avoidance behavior was facilitated in rats exposed to a phase-shifted illumination cycle, but social and explorative behavior of rats tested in dyadic encounters were not affected by changing the normal illumination cycle. It is concluded that phase-shifting may result in amnesia for newly learned behavioral responses, but not for more innate behavioral patterns.

Amnesia↗
PubMed1985

The roles of information reactivation and nonassociative arousal in recovery from ECS-induced retrograde amnesia.

Restoration of memory by pretest reminder treatments following ECS-induced amnesia in principle could be mediated by nonassociative arousal and/or reactivation of information by the reminder stimuli. In the present research, arousal value of the reminder treatment was largely a function of the novelty of the context in which the reminder cues occurred. After producing ECS-induced amnesia in rats for a signaled passive avoidance task, presentation of the signal outside of the training and test context proved to be an effective reminder cue. However, prereminder familiarization with the reminder location, which was sufficient to reduce exploratory behavior suggestive of a decrease in the arousal value of the context, did not influence recovery from amnesia. These data indicate that reminder treatments are capable of reversing experimental amnesia by initiating further processing of previously acquired information even when the treatment does not produce appreciable arousal.

Amnesia↗
PubMedDate not supplied

Hippocampal monoamine metabolism and the CO2 induced retrograde amnesia gradient in rats.

It was found that in rats a gradient of retrograde amnesia for a passive avoidance response could be established when carbon dioxide (CO2) was used as the amnesic agent. The extent of passive avoidance increased as the period between application of a mild foot shock and CO2 treatment was increased. The amnesia gradient was found to cover a period of at least 60 min. Changes in hippocampal serotonin metabolism parallelled the amnesia gradient. Thus, the concent increased. The changes in hippocampal noradrenaline and dopamine did not correlate with the amnesia gradient.

Amnesia↗
PubMed1985

The neuropathology of amnesia.

Relations between brain damage and memory disturbance are outlined with emphasis on the so-called amnesic syndrome. Following a brief introduction into forms of memory and memory failures, the basic causes of brain damaage (with relevance to amnestic failures) are described. Thereafter, the two best-known forms of brain damage-amnesia relations are reviewed: the consequences of damage to medial temporal lobe structures and to diencephalic regions. For the cases with medial temporal lobe damage, evidence is reported in greater detail for H.M., who has been examined more than any other amnesic patient for more than 30 years now, as a considerable amount of literature has accumulated on his behavior in diverse situations. Other cases with more or less circumscribed damage to medial temporal lobe structures are reviewed so as to outline criteria for or against the hypothesis that there are regions within the medial temporal lobe whose damage might be critical for the amnesic syndrome. Two cases of diencephalic amnesia are summarized in particular (cases of Mair et al., 1979) as they have received extensive neuropsychological and neuropathological investigation. Other cases with, for example, Korsakoff's disease are reviewed, as well as cases with diencephalic, or combined mesencephalic-diencephalic damage without nutritional causes. A third group of patients with massive, but still selective amnesic disturbances are then described: cases of basal forebrain damage, followed by descriptions of Alzheimer's disease which has similarities in the underlying neuropathology. This leads over to cases with more generalized intellectual deteriorations (dementia), which may have developed on the basis of primarily cortical damage or damage principally to basal ganglia structures. After reviewing cases with mainly material-specific memory failures--usually as a consequence of restricted neocortical damage--a separate section follows on patients in whom retrograde amnesia is the prominent symptom. The contribution of animal models of human amnesia is critically reviewed and discrepancies are analyzed between human and animal memory disturbances. This section emphasizes the value of investigating inter-dependencies between brain structures by pointing out that relations between memory disturbances and brain damage may be more complicated than apparent from a simple structure-function assignment. This aspect is further followed up in the conclusions.

Alcohol Amnestic Disorder↗
PubMed1980

Persistent retrograde memory deficit after transient global amnesia.

A 64-year-old woman suddenly had an attack of confusion and amnesia that suggested transient global amnesia. However, her loss of memory for recent events lasted more than ten days and was accompanied by psychomotor agitation and transient alteration of sexual behavior. The patient had no other neurologic signs during the episode. She recovered completely from the recent memory deficit, but was left with a persistent retrograde amnesia for a period of five to ten years and total amnesia for the acute episode. The EEG was suggestive of a left medial temporal lobe lesion.

Amnesia↗
PubMed1984

[Post-traumatic retrograde amnesia].

A case of post traumatic retrograde amnesia is described. The patient presented after an initial coma a global amnesia, but the fixation deficit rapidly disappeared, and a severe retrograde amnesia dating back to childhood experience and learning remained the main symptom. Amnesia for remote events was associated with didactic memory deficit and, at a lesser degree, with a verbal memory deficit. Recovery of fixation allowed a progressive relearning. This pattern of impairment was recently related to mesencephalic lesions, but we think that the role of temporal lobe involvement cannot be neglected.

Adult↗
PubMed2002

Focal retrograde amnesia documented with matching anterograde and retrograde procedures.

Focal retrograde amnesia is an unusual and theoretically challenging form of memory disorder. The case of a 65-year-old woman presenting with focal retrograde amnesia is reported. Following a cardiac arrest and subsequent hypoxia she remained in a coma for 24 h with evidence of epileptiform activity during the early recovery period. MR scans, 4 and 7 months post-onset, showed mild bifrontal atrophic changes mainly affecting white matter areas. An [18F]fluorodeoxyglucose resting PET scan 1-year post-onset demonstrated right occipito-temporo-parietal hypometabolism. We were able to document the patient's performance on an extensive range of anterograde and retrograde tests and to monitor her recovery of function by assessing her performance at 4, 12 and 24 months post-onset. Spared anterograde memory was observed on a range of verbal and non-verbal tests, including matched tasks that compared pre-illness and post-illness onset recollections. In contrast, her performance on retrograde memory tests, using detailed autobiographical and public events verbal and photographic tasks, showed a temporally-graded retrograde amnesia, more particularly affecting memory for autobiographical episodes. Possible mechanisms underlying CH's focal retrograde amnesia are discussed in terms of Damasio's time-locked multiregional retroactivation model.

Aged↗
PubMed1987

Stability of long temporal gradients of retrograde amnesia in mice.

Mice were given a single training trial and then received a series of four electroconvulsive shocks (ECS), 1 h apart, at one of several times after training (1-180 days). Retention was then tested at one of three times after ECS: 7, 14, or 28 days. Control animals that received sham treatment exhibited gradual forgetting with increasing training-retention intervals. Mice given ECS exhibited temporally graded retrograde amnesia, which affected memories acquired up to about 14 days before treatment. The retrograde amnesia was relatively stable, maintaining its temporally graded appearance for at least 28 days after ECS. Some recovery may have occurred in the case of memories acquired 7 days or longer before ECS, but memories acquired only 1 or 5 days before ECS did not recover. These findings extend the parallel between experimental amnesia in laboratory animals and human amnesia.

Amnesia↗
PubMed1989

Observations during transient global amnesia. A behavioural and neuropsychological study of five cases.

The clinical and behavioural features of 5 patients examined during transient global amnesia (TGA) are described. All underwent extensive neuropsychological testing during and sequentially after the attack. Our results show that in TGA there is a characteristic neuropsychological deficit which parallels that in the permanent amnesic syndrome. Personality, complex cognition and problem solving, semantic knowledge, language and visuospatial function remained intact. Immediate memory was preserved. Longer-term verbal and nonverbal memory was severely disrupted in all cases. In contrast, the extent of retrograde amnesia was highly variable. A famous faces test showed an extensive deficit in 3 cases, with improvement in all cases following the attack. Analysis of group data confirmed the presence of a reversible temporal gradient, in that more distant memories were relatively spared. On a famous events test, recognition was normal across all decades, but dating of events from the 1960s and 1970s was consistently impaired. The Crovitz test of remote personal episodic memory was given to 3 subjects; all showed impaired uncued autobiographical memory and in contrast to normal controls, had a virtual absence of recent memories. During recovery from TGA there was progressive shrinkage of retrograde amnesia but a permanent short retrograde gap of around 1 h remained in all cases. Although subjectively normal within 24 h, all cases demonstrated persisting impairment of new learning for at least a week post-TGA. The relevance of the neuropsychological data to theories concerning the amnesic syndrome is discussed. We postulate a temporary deficit in retrieval of remote memories which appears to be dissociable from the anterograde amnesia.

Aged↗
PubMed1984

Transient global amnesia: neuropsychological dysfunction during attack and recovery in two "pure" cases.

Two patients with transient global amnesia are reported. Comprehensive neuropsychological evaluation, during the amnesic episode, as well as follow-up examinations on memory were performed. The course of the amnesia was exemplified by two comparable memory tests in different modalities. Partial retrograde amnesia and complete anterograde amnesia were demonstrated during the transient episode. Objective recovery was found to be slower than subjectively experienced, but test performance was completely normal one month after onset.

Adult↗
PubMed1987

Transient global amnesia and epilepsy. Electroencephalographic distinction.

Electroencephalographic recordings were obtained during 13 episodes of transient global amnesia in 13 patients. Eight were entirely normal; none showed seizure discharges or other epileptiform activity. Electroencephalographic recordings were also obtained after 103 episodes of amnesia in 96 patients with transient global amnesia (TGA) alone, five patients who had both TGA and epilepsy independently, and three patients with amnesia related to epilepsy. The majority (60.8%) of waking records were normal during or after episodes of TGA. Mild or moderate and nonfocal abnormalities were found in a minority. Genuine epileptiform activity was observed only among patients who had seizure disorders. Amnestic episodes attributable to seizures were more brief and more apt to be repeated than TGA and usually responded to anticonvulsant drugs. Differentiation of TGA from epilepsy is essential for appropriate management.

Amnesia↗
PubMed1989

Procedural memory during posttraumatic amnesia in survivors of severe closed head injury. Implications for rehabilitation.

To investigate the possibility that learning of skills (ie, procedural memory) is preserved during posttraumatic amnesia, 16 amnesic survivors of severe closed head injury and 16 control subjects were studied. Procedural learning tasks included mirror reading, mazes, and a pursuit rotor task that involved tracking a rotating target. Declarative memory was assessed by testing recognition of the words used in mirror reading and a questionnaire concerning details of the previous testing session. Learning was evaluated on 3 consecutive days and a fourth session was scheduled after resolution of posttraumatic amnesia. Despite stable impairment of declarative memory during posttraumatic amnesia, the performance of head-injured patients improved across sessions on all procedural tasks and showed transfer to testing after resolution of posttraumatic amnesia.

Adolescent↗
PubMed1985

Amnesia in monkeys after lesions of the mediodorsal nucleus of the thalamus.

Recent successes in developing an animal model of human amnesia in the monkey have made it feasible to try to identify with certainty the specific structures in the diencephalon and medial temporal region that cause amnesia when damaged. Monkeys with small lesions restricted largely to the posterior portion of the mediodorsal nucleus of the thalamus were given a test of memory sensitive to human amnesia and a second test that is analogous to the skill-based tasks performed normally by amnesic patients. The monkeys exhibited a marked impairment on the first test and performed normally on the second. The results show that circumscribed lesions of the mediodorsal nucleus can cause substantial amnesia.

Amnesia↗