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PubMed1986

The prognosis of transient global amnesia. Results of a multicenter study.

In a Danish multicenter study, 74 patients 20 to 75 years of age (mean age, 58.8 years) with transient global amnesia (TGA) without accompanying major neurological signs were studied. Over a follow-up period ranging from seven to 210 months (mean, 66.6 months) the observed rates of death and cerebrovascular morbidity were similar to those expected in the Danish population, matched for age and sex. Sixteen patients (22%) had further TGAs occurring one month to nine years after the original episode; the mean annual recurrence rate was 4.7%. We concluded that TGA without associated major neurological deficits is a benign clinical phenomenon, probably caused by a functional cerebral disturbance unrelated to cerebrovascular disease in general. Furthermore, the observed temporal pattern of recurrence suggests that, although TGA is in principle a recurrent disorder, the annual risk of recurrence is so low that most of the elderly patients are likely to experience only one attack.

Adult↗
PubMed2001

Anterograde and retrograde amnesia in rats with large hippocampal lesions.

A test of socially acquired food preferences was used to study the effects of large lesions to the hippocampal formation (HPC) on anterograde and retrograde memory in rats. In the anterograde test, rats with HPC lesions normally acquired the food preference but showed a faster rate of forgetting than control groups. When the food preference was acquired preoperatively, HPC groups exhibited a temporally graded retrograde amnesia in which memory was impaired when the preference was acquired within 2 days of surgery but not at longer delays. The results support the traditional theory that the HPC contributes to the consolidation of newly acquired information into a durable memory trace that is represented in other brain areas. Consistent with this view, the results indicate that, once a memory trace is consolidated, the HPC does not participate in its storage or retrieval. The possibility is considered that extrahippocampal areas in the medial temporal lobe are needed to maintain a memory trace throughout its existence.

Amnesia, Anterograde↗
PubMed1986

Phencyclidine-induced retrograde amnesia in mice.

The amnesic action of phencyclidine (PCP) was investigated in mice using a passive avoidance- and escape-learning method. PCP (10-30 mg/kg) administered immediately after the training test dose-dependently shortened and prolonged the step-down latency and escape latency, respectively in the retention test. There was a significant inverse relationship between the step-down and escape latencies, indicating that PCP had induced amnesia. The amnesic actions of PCP were retrograde, being observed when mice were given PCP within 10 min but not more than 30 min after the training test. The amnesic effects of PCP on both variables were antagonized significantly by physostigmine and naloxone, whereas cyproheptadine and haloperidol had no effect. None of these drugs by themselves affected passive avoidance- or escape-learning performance. These results suggest that the retrograde amnesic actions of PCP were produced via either the cholinergic or the opioidergic systems or both, but not through the serotonergic and the dopaminergic systems.

Amnesia↗
PubMed1980

Beta-endorphin causes retrograde amnesia and is released from the rat brain by various forms of training and stimulation.

The endogenous opiate peptide, beta-endorphin (0.4, 1.0, 2.0, and 10.0 microgram/kg) was injected IP into rats immediately after training in a shuttle avoidance task, and its effect on memory retention was evaluated in test sessions carried out 24 h later. The drug was found to cause retrograde amnesia, the ED50 being 1.0 microgram/kg. Beta-endorphin immunoreactivity was measured in the hypothalamus and rest of the brain of rats submitted to training, or test sessions of shuttle avoidance learning, pseudoconditioning in the shuttle-box, tones alone, or foot-shocks alone. After training in any of the four paradigms, there was a marked (46-60%) depletion of beta-endorphin immunoreactivity in the rest of the brain. No changes were detected in the hypothalamus or after test sessions. The loss of beta-endorphin immunoreactivity may be attributed to release of this substance caused by the stimuli used for training. From the present findings, as well as previous observations on the memory-facilitating influence of the opiate receptor antagonist, naloxone, it is concluded that there is a physiological amnesic mechanism mediated by beta-endorphin (and perhaps other opoid peptides as well), which is triggered by the non-associative factors present in the various forms of learning.

Amnesia↗
PubMed1988

Transient global amnesia and migraine.

Formal neuropsychological evaluation in patient with transient global amnesia (TGA) associated with migraine was performed 6 days and 17 months after the episode. Verbal learning difficulties and verbal IQ deficit were observed in line with the neuropsychological profile seen in the follow-up of TGA. A common origin for the TGA-Migraine episode and isolated TGA is discussed.

Amnesia↗
PubMed1988

Amnesia for the McCollough effect following unilateral electroconvulsive therapy: implications for laterality.

The hemispheric lateralization of retrograde amnesia following unilateral electroconvulsive therapy (ECT) was measured by a novel nonverbal probe, the McCollough effect, which allowed equal and exclusive access to each hemisphere. Alternating exposure to perpendicular gratings of complementary colors (e.g., red vertical stripes alternated with green horizontal stripes) will cause subsequently presented black and white gratings to appear colored hours or even days later (the McCollough effect). Three of the patients examined (3 of 10) lost the effect in just the half visual field contralateral to the treatment side when unilateral nondominant ECT was interposed between the induction of the effect and the its test. Six patients lost the effect bilaterally following unilateral ECT. One patient retained a bilateral aftereffect. This patient had by far the shortest seizure (18 sec). Nine of 10 comparison patients, also suffering from major depression but without ECT intervening between induction and test, showed good bilateral retention of the McCollough effect. The remaining comparison patients showed no retention. These results imply that despite bilateral cortical spread of seizure activity, unilateral nondominant ECT has effects that are most pronounced over the stimulated hemisphere.

Adult↗
PubMed1983

The anterograde and retrograde retrieval ability of a patient with amnesia due to encephalitis.

A patient with amnesia due to encephalitis was previously described in 1976 as having normal short-term memory and an intact ability to perform semantic analysis. Despite this ability, his retention beyond the limits of short-term memory was nearly nil. The present investigation sought to evaluate more completely the nature of this patient's retrieval deficit using a series of paradigms developed subsequent to his initial testing. Once again it was discovered that while his intact analytic abilities allowed retention of material in working memory, as soon as that working capacity was exceeded, retrieval of information became nearly impossible. It became apparent that the patient could not discriminate between a cue's most recently analyzed associate and the strongest existing associate to that cue in his semantic hierarchy. An analysis of his retrograde memory ability showed that he could retrieve almost no real episodes of either a public or private nature from his past. Instead, he seemed to rely on generalizations from his semantic memory to reconstruct "probable" events.

Amnesia↗
PubMed1975

Effects of prior aversive experience upon retrograde amnesia induced by hypothermia.

Two experiments examined the extent to which retrograde amnesia (RA) is attenuated by prior learning experiences. In Experiment 1, rats initially received either passive avoidance training in a step-through apparatus, exposure to the apparatus, or noncontingent footshock. When training on a second but different passive avoidance task was followed by hypothermia treatment, RA was obtained only in the latter two groups. In Experiment 2, one-way active avoidance training, yoked noncontingent shocks, or apparatus exposure constituted the initial experience. Subsequent step-down passive avoidance training and amnestic treatment resulted in memory loss for the prior apparatus exposure group, but not for either of the preshocked conditions. These experiments demonstrate that certain types of prior aversive experience can substantially modify the magnitude of RA, and, in conjunction with other familiarization studies, emphasize a paradox for interpretations of RA based solely upon CNS disruption. The possibility that hypothermia treatment serves as an important contextual or encoding cue necessary for memory retrieval was considered. It was suggested that prior experience may block RA by enabling rats to differentiate training and treatment conditions.

Amnesia↗
PubMed1976

Reversal of amnesia by an orally active ACTH 4-9 analog (Org 2766).

The ACTH 4-9 analog, H-Met((O2)-Glu-His-Ph-D-Lys-Phe-OH (Or 2766), attenuates in rats CO2-induced amnesia for a one-trial passive avoidance step-through response when administered prior to the retrieval test but not when given prior to acquisition. Even a dose of 0.001 mug/rat Org 2766 yields an anti-amnesic effect. In this respect Org 2766 is more active than the ACTH fragment ACTH 4-10. An anti-amnesic effect was also obtained when Org 2766 was administered orally. ACTH 4-10 (100 mug/rat) has to be given SC within 8 hr of the retrieval test in order to be effective. A similar time span of effectiveness was observed when Org 2766 was SC injected in a dose of 0.1 mug/rat. The anti-amnesic effect of ACTH 4-10 remains when the time interval between acquisition and retrieval is extended beyond the usual 24 hr. The same appeared to be true for SC ADMINISTERED Org 2766. It is suggested that ACTH-like peptides, and particularly the orally active Org 2766, may be helpful in the treatment of deficient mental performance.

Administration, Oral↗
PubMed1977

Retrograde amnesia production by the intracisternal injection of 20 micronl of saline in rats.

The intracisternal injection of 20 micronl of saline into a rat within an hour after training it in an active avoidance response was found to induce retrograde amnesia. The results obtained by combining this procedure with the intracisternal injection of 2,6 Diaminopurine (DAP), which inhibits RNA synthesis and prevents long-term memory formation when administered at the proper time and in the correct dosage, suggest the existence of a medium term memory (MTM) mechanism. MTM was normally evident up to 75 min after training but was demonstrable up to 210 min when LTM formation was prevented by DAP.

2-Aminopurine↗
PubMed1982

Intracerebroventricular administration of nanogram amounts of beta-endorphin and Met-enkephalin causes retrograde amnesia in rats.

The intracerebroventricular (icv) administration of 5.0 or 25.0 ng of beta-endorphin or Met-enkephalin causes retrograde amnesia for a shuttle avoidance task ion rats. In both cases, the higher dose was more effective than the lower one. The present results confirm previous similar findings obtained using systemic administrations of these compounds, and suggest that the amnestic effect of beta-endorphin and Met-enkephalin is mediated centrally.

Amnesia↗
PubMedDate not supplied

The ACTH-(4-9) analog ORG 2766 and desglycinamide9-(Arg8)-vasopressin reverse the retrograde amnesia induced by disrupting circadian rhythms in rats.

Disrupting circadian organization by exposing rats to a shifted illumination schedule after training for passive avoidance and shuttle box avoidance behavior resulted in retrograde amnesia as evidenced by impaired performance during retention and extinction testing respectively. A single treatment with either the ACTH-(4-9) analog ORG 2766 or desglycinamide9-(Arg8)-vasopressin (DGAVP) 1 hour prior to the retention of passive avoidance or extinction of shuttle box avoidance behavior restored the behavioral impairment. It is suggested that these peptides may be useful to relieve memory deficits induced by disturbances in circadian organization.

Adrenocorticotropic Hormone↗
PubMed1981

Retrograde amnesia caused by Met-, Leu- and des-Try-Met-enkephalin in the rat and its reversal by naloxone.

Immediate post-training i.p. injection of Met-enkephalin, Leu-enkephalin or des-Tyr-Met-enkephalin, caused retrograde amnesia for a shuttle avoidance task in rats. The effect was linearly related to the log of the dose between 0.32 and 2.0 microgram/kg, and the potency of the three compounds was similar (ED50 0.35-0.45 microgram/kg). Naloxone (0.2 mg/kg) antagonized the amnestic effect of the peptides. Since the log dose-response curves were displaced to the right in quasi-parallel fashion, and Lineweaver-Burk plots of the data showed an intersection very close to the origin of the horizontal axis, the antagonism between naloxone and the three peptides appears to be competitive.

Amnesia↗
PubMed1989

Retrograde amnesia induced by lidocaine injection into the striatum: protective effect of the negative reinforcer.

A variety of manipulations which interfere with the activity of the striatum, including cholinergic blockade and spreading depression, produce amnesia. However, it has been demonstrated that with overtraining, striatal spreading depression and injections of anticholinergic drugs do not produce memory deficits in positively-rewarded tasks. In the present experiment 2% lidocaine was injected into the striatum shortly after training of passive avoidance, using three levels of footshock (0.2, 0.3, and 0.4 mA). Highly significant retention deficits were produced when the lower intensities were studied; in contrast, the animals trained with 0.4 mA showed near-perfect performance. The data show that the enhanced learning experience, which may be equivalent to overtraining, also protects against memory deficits in negatively-rewarded behaviors, and suggest that it induces a transfer of mnemonic functions from the striatum to other neural structures.

Amnesia↗
PubMed1989

Focal retrograde amnesia: a long term clinical and neuropsychological follow-up.

A patient (E.D.) who had displayed a selective retrograde amnesia in association with transient amnesic episodes (Kapur et al., 1986) was reexamined five years after initial assessment. At the clinical level, his transient amnesic attacks continued, but some of these had clear epileptic features. In addition, EEG investigation indicated temporal lobe abnormality, more prominent in the left temporal region, and supported a clinical diagnosis of temporal lobe epilepsy. Both CT scanning and magnetic resonance imaging were unable to detect the presence of any structural lesion. At the neuropsychological level, there was no evidence of dementia in the form of generalized cognitive dysfunction nor significant deterioration in cognitive functioning since the earlier assessment. Our patient continued to show marked memory loss for public events over the past 20-30 years, in the context of normal or near normal performance on most tests of anterograde memory functioning. While memory for famous scenes and famous faces was markedly impaired, our patient's memory for famous cars was within normal limits and his memory for autobiographical events showed only patchy impairment. Although E.D. performed at an average or above average level on most standard tests of anterograde memory functioning, our patient did show evidence of significant memory loss for public events which had occurred over the past ten years (i.e. since the onset of his illness). The possibility is raised that E.D.'s memory disorder may represent a form of disconnection syndrome.

Aged↗
PubMed1986

Studies on retrograde and anterograde amnesia of olfactory memory after denervation of the hippocampus by entorhinal cortex lesions.

The effect of hippocampal denervation on olfactory memory in rats was tested after interrupting the lateral olfactory tract projections at the level of the entorhinal cortex. When lesioned animals were trained to learn new odors, they showed no evidence of retention 3 h after acquisition. These results confirm earlier data on rapid forgetting in rats after hippocampal deafferentation and are in parallel to the anterograde amnesia typically found in humans with hippocampal damage. On the other hand, preoperatively learned information was minimally impaired after hippocampal deafferentation even if it was acquired within less than 1 h before the lesion. This finding differs from reports on humans as well as monkeys with hippocampal damage where memories formed during a critical time span of months or even years before the lesion are found to be impaired. This may suggest that the consolidation process in humans and rodents has different time scales or that the roles of the human and the rat hippocampal structure in memory formation are somewhat different.

Amnesia↗
PubMedDate not supplied

Retrograde amnesia in patients with Alzheimer's disease or Huntington's disease.

Retrograde amnesia (RA) was studied in patients with Huntington's disease (HD) or Alzheimer's disease (AD) using an updated version of the remote memory battery originally developed by Albert, Butters and Levin. Regardless of whether remote memory was measured by unaided recall or cued recall, HD patients exhibited deficits that were equally severe across decades. RA was more severe in AD than in HD patients and the AD patients recalled significantly more items from the 1940s and 50s than from the 60s, 70s or 80s. The AD patients also displayed dysnomia, while the HD patients did not. Naming difficulties appeared to contribute to the poor overall performance of the AD patients, but did not account for the temporal gradient of their RA. These findings, like recent reports focusing on these patients' ability to learn new information and to search semantic memory, indicate that the processes underlying AD and HD patients' memory failures are distinct.

Adult↗