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PubMed1981

Phase shifting circadian rhythms produces retrograde amnesia.

Phase shifting circadian rhythms in rats shortly after passive avoidance training impaired their performance on retention tests. The amnesia was not due to simple performance deficits accompanying the "jet leg" effects of phase shifting or to differences in lighting or circadian phase at training and at testing. Amnesia was associated with specific rhythm reentrainment patterns. These data indicate that disrupting circadian organization can produce retrograde amnesia in rats.

Amnesia↗
PubMed1977

Long-term effects of prior experience in attenuating amnesia.

In Experiment I, prior experience with passive-avoidance training followed by latent extinction was given 1, 3, 5, or 15 days before criterion (re) training and an amnesic treatment. It produced nearly complete protection from retrograde amnesia at the three shorter intervals; at the longest interval, amnesia was present but less severe than in a control group without the familiarization. In Experiment II, prior experience was given 1, 5, or 15 days before a noncontingent shock and an amnesic treatment. Evidence of a reactivation of memory was obtained only at the longest interval. Thus, familiarization and reactivation seem to represent different processes. The results are interpreted as consistent with explanations stressing the disruption of retrieval in retrograde amnesia.

Amnesia↗
PubMed1984

Transient global amnesia due to clioquinol.

Twelve cases of confusional state after normal or excessive doses of clioquinol are discussed. They resemble transient global amnesia (TGA) of the classic type, but the episodes last longer (1-3 days), they are often accompanied by a variety of mental disturbances, and the onset and end are less well defined than in the classic type. A combination of SMON and acute encephalopathy due to clioquinol was observed in only one case. Apart from amnesia for the acute episode a permanent retrograde amnesia for a few days up to two months was left behind. The pathophysiology of these episodes is not clear, but they resemble the toxic reactions to clioquinol observed in dogs and experimental animals.

Acute Disease↗
PubMed1982

Transient global amnesia after cerebral angiography. Report of seven cases.

Because of a case of typical transient global amnesia following cerebral angiography, the records of all patients undergoing cerebral angiography during a seven-year period were reviewed. Six other cases were discovered. All patients had either transfemoral catheter or brachial angiograms performed immediately before the development of amnesia. Spasm of a vertebral artery was noted in one case. None had clinically obvious seizures. All recovered within 24 hours. This only recently reported complication of cerebral angiography is consistent with a vascular etiology of the syndrome of transient global amnesia when not associated with angiography, although a direct toxic effect of the contrast material cannot be excluded.

Acute Disease↗
PubMed2004

Recovery of anterograde amnesia in a case of craniopharyngioma.

BACKGROUND: Studies of the amnesic syndrome have indicated that telencephalic and diencephalic structures are critical components of the memory system. The exact role of the mammillary bodies (MBs) in human memory remains elusive, since few cases of selective MB damage have been reported. OBJECTIVE: To study a case of severe anterograde amnesia due to a third-ventricle craniopharyngioma with severe MB compression. DESIGN: Case report. SETTING: Neurosurgery clinic of an academic hospital. PATIENT: A 53-year old woman who developed severe anterograde amnesia due to a third-ventricle craniopharyngioma strongly compressing the MBs and, to a lesser extent, the right hippocampus. INTERVENTIONS: Surgical excision of the tumor and neuropsychological testing and positron emission tomography during an associative memory test before and 2 months after tumor removal. A postsurgical magnetic resonance image did not show evidence of damage to the hypothalamus, thalamus, hippocampus, or MBs. MAIN OUTCOME MEASURES: Changes in brain imaging data and results of neuropsychological testing. RESULTS: After tumor removal, the patient showed a complete recovery of memory functions. Performance on the associative memory test was at chance level before surgery and dramatically improved postoperatively. Results of the preoperative positron emission tomographic study showed no activity in memory-related structures. In contrast, a significant blood flow increase occurred in the anterior thalamic nuclei postoperatively. CONCLUSIONS: These behavioral and brain imaging data stress the importance of the MBs in this patient's amnesia. Our data further suggest that the clinical prognosis of decompressing the mammillothalamic tract is excellent, even in cases of massive compression.

Amnesia, Anterograde↗
PubMed1998

Episodic memory, semantic memory, and amnesia.

Episodic memory and semantic memory are two types of declarative memory. There have been two principal views about how this distinction might be reflected in the organization of memory functions in the brain. One view, that episodic memory and semantic memory are both dependent on the integrity of medial temporal lobe and midline diencephalic structures, predicts that amnesic patients with medial temporal lobe/diencephalic damage should be proportionately impaired in both episodic and semantic memory. An alternative view is that the capacity for semantic memory is spared, or partially spared, in amnesia relative to episodic memory ability. This article reviews two kinds of relevant data: 1) case studies where amnesia has occurred early in childhood, before much of an individual's semantic knowledge has been acquired, and 2) experimental studies with amnesic patients of fact and event learning, remembering and knowing, and remote memory. The data provide no compelling support for the view that episodic and semantic memory are affected differently in medial temporal lobe/diencephalic amnesia. However, episodic and semantic memory may be dissociable in those amnesic patients who additionally have severe frontal lobe damage.

Amnesia↗
PubMed1999

Temporally-specific retrograde amnesia in two cases of discrete bilateral hippocampal pathology.

The role of the hippocampus in retrograde amnesia remains controversial and poorly understood. Two cases are reported of discrete bilateral hippocampal damage, one of which was a rare case of limbic encephalitis secondary to the human herpes virus 6. Detailed memory testing showed marked anterograde memory impairment, but only mild, temporally-limited retrograde amnesia that covered a period of several years in both autobiographical and factual knowledge domains. The absence of extensive retrograde amnesia in these two cases points to a time-limited role for the hippocampus in the retrieval of retrograde memories, and suggests that entorhinal, perirhinal, parahippocampal, or neocortical areas of the temporal lobe may be more critical than the hippocampus proper for long-term retrograde memory functioning. Our findings offer general support to theories of memory consolidation that propose a gradual transfer of memory from hippocampal to neocortical dependency.

Adult↗
PubMed2001

Retrograde amnesia after hippocampal damage: recent vs. remote memories in two tasks.

We review evidence from experiments conducted in our laboratory on retrograde amnesia in rats with damage to the hippocampal formation. In a new experiment reported here, we show that N-methyl-D-aspartate (NMDA)-induced hippocampal damage produced retrograde amnesia for both hidden platform and two-choice visible platform discriminations in the Morris water task. For both problems there was a significant trend for longer training-surgery intervals to be associated with worse retention performance. Little support is offered by our work for the concept that there is a process involving hippocampal-dependent consolidation of memories in extrahippocampal permanent storage sites. Long-term memory consolidation may take place within the hippocampus. The hippocampus may be involved permanently in storage and/or retrieval of a variety of relational and nonrelational memories if it was intact at the time of learning, even involving information which is definitely not affected in anterograde amnesia after hippocampal damage.

Amnesia, Retrograde↗
PubMed2001

Retrograde amnesia and consolidation: anatomical and lesion considerations.

The four papers in this issue of Hippocampus dealing with retrograde amnesia, together with relevant animal studies in the literature, are reviewed from the perspective of the anatomical location of the lesion and extent of damage to the brain. In order to evaluate the underlying damage in these and related prospective experimental studies, it is necessary to consider both the lesion techniques that were used as well as the care with which the resulting damage was determined. Both temporally graded and flat, ungraded retrograde amnesia have been reported, as well a lack of effects, following damage to structures in the medial temporal area. Most research has centered around damage to the hippocampus, but differences in selectivity of the lesions and behavioral testing procedures preclude any definite conclusions regarding the precise nature of the involvement of this structure. With a greater appreciation for the importance of the locus and extent of the damage, together with the kind of information being processed, it should be possible to obtain a better understanding of the neural substrates underlying retrograde amnesia.

Amnesia, Retrograde↗
PubMed2005

Competitive interactions between endogenous LTD and LTP in the hippocampus underlie the storage of emotional memories and stress-induced amnesia.

This speculative review serves two purposes. First, it as an extension of the ideas we developed in a previous review (Diamond et al., Hippocampus, 2004;14:281-291), and second, it is a rebuttal to Abraham's (Hippocampus, 2004;14:675-676) critique of that review. We had speculated on the functional significance of the finding that post-training LTP induction produces retrograde amnesia. We noted the similarities between the findings that strong tetanizing stimulation can produce LTP and retrograde amnesia, and that a strong emotional experience can produce a long-lasting memory and retrograde amnesia, as well. The commonalities between LTP induction and emotional learning provided the basis of our hypothesis that an emotional experience generates endogenous LTD/depotentiation, which reverses synaptic plasticity formed during previous learning experiences, and endogenous LTP, which underlies the storage of new information. Abraham raised several concerns with our review, including the criticism that our speculation "falters because there is no evidence that stress causes LTD or depotentiation," and that research on stress and hippocampus has "failed to report any LTP-like changes." Abraham's points are well-taken because stress, in isolation, does not appear to generate long-lasting changes in baseline measures of hippocampal excitability. Here, within the context of a reply to Abraham's critique, we have provided a review of the literature on the influence of stress, novelty, fear conditioning, and the retrieval of emotional memories on cognitive and physiological measures of hippocampal functioning. An emphasis of this review is our hypothesis that endogenous forms of depotentiation, LTD and LTP are generated only when arousing experiences occur in conjunction with memory-related activation of the hippocampus and amygdala. We conclude with speculation that interactions among the different forms of endogenous plasticity underlie a form of competition by synapses and memories for access to retrieval resources.

Amnesia, Retrograde↗
PubMed1997

Antibody to day-old chick brain glycoprotein produces amnesia in adult rats.

Polyclonal antibody R-1, raised against a chick synaptic membrane glycoprotein fraction whose synthesis is enhanced following training on a passive avoidance task, produces amnesia when injected into chick forebrain 5.5 h posttraining. The amnestic IgG fraction specifically recognizes a low sialylated isoform of NCAM (Mileusnic Rose, Lancashire, & Bullock, 1995). We have now investigated the effects of this antibody on memory formation in adult rats. R-1, preimmune serum, or saline was injected intracerebroventricularly 5.5 h posttraining through bilaterally implanted cannulae. Rats injected with R-1 and tested 48 h later showed a significant amnesia for avoidance compared with the controls. Amnesia was not apparent at 24 h posttraining. R-1 injections were without effect on spontaneous locomotor or exploratory activity in a holeboard test. The results contribute to the argument that the role of cell adhesion molecules in neuronal plasticity is not limited to the developing nervous system, but they play a more general role in the experience-dependent synaptic remodeling underlying long-term memory.

Amnesia↗
PubMed1986

Retrograde memory enhancement by diazepam: its relation to anterograde amnesia, and some clinical implications.

The effect of diazepam on retention of an inhibitory avoidance task was investigated in mice. In Experiment 1, animals were trained in this task, and tested for retention 24 h later. The mice received, 20 min after training, an IP injection of either diazepam (2 mg/kg) or saline; half of the mice in each treatment group were exposed, 40 min after avoidance training (and 20 min after the injections) to a Y maze. Exposure to the Y maze disrupted retention of the avoidance task in the saline-treated animals, and enhanced it in the diazepam-treated mice. Retention of habituation to the Y maze was impaired in the diazepam group. The effect can be explained by an interaction of the drug with the Y maze, by which exposure to the Y maze became facilitatory, instead of deleterious, to retention of the avoidance task. This may or may not be related to anterograde amnesia for the Y maze; and may be related to effects of diazepam seen in clinical practice. In Experiment 2, diazepam was given prior to, instead of after, inhibitory avoidance training; it caused anterograde amnesia for this task, which was not reversed by pre-test diazepam, and was therefore not due to state dependency. In conclusion, the effect of diazepam on inhibitory avoidance learning depends on the time at which the drug is given. A pretraining injection causes amnesia, whereas a post-training injection, while ineffective per se, may facilitate retention of the task when it is followed by exposure to a habituation procedure.

Amnesia↗
PubMed1992

Effects of nefiracetam, DM-9384 on amnesia and decrease in choline acetyltransferase activity induced by cycloheximide.

The effects of nefiracetam, [N-(2,6-dimethyl-phenyl)-2-(2-oxo-pyrrolidinyl)acetamide, DM-9384], a cyclic derivative of GABA, were investigated in the cycloheximide (CXM)-induced amnesia animal model using the passive avoidance task. Pre-training administration of DM-9384 attenuated the CXM-induced amnesia as indicated by prolongation of step-down latency. It protected against CXM-induced inhibition of choline acetyltransferase activity in the cerebral cortex. These results suggest that DM-9384 attenuates CXM-induced amnesia by interacting with AChergic neuronal system and enhancing protein synthesis in the brain.

Amnesia↗
PubMed1994

Nootropic effect of nicotine on carbon monoxide (CO)-induced delayed amnesia in mice.

The effects of nicotine on carbon monoxide (CO)-induced amnesia in mice were investigated using a step-down type passive avoidance task. Mice were exposed to CO 3 times at 1-h intervals, 7 days before the first training and retention test and 24 h after the first training session. Memory deficiency occurred in mice when training commenced more than 3 days after CO exposure (delayed amnesia): the median step-down latency in the retention test of the CO-exposed group was significantly shorter than that of the control group. Administration of (-)-nicotine (15.6 and 31.3 nmol/kg, IP) 15 min before the first training session prolonged the step-down latency in the CO-exposed group, but (+)-nicotine did not. To determine whether this effect of (-)-nicotine was mediated via nicotinic cholinergic receptors, we attempted to block its action using a nicotinic acetylcholine receptor antagonist (mecamylamine). Mecamylamine (1.25 mumol/kg) blocked the effect of (-)-nicotine (31.3 nmol/kg) on delayed amnesia. Administration of (-)-nicotine (15.6-62.5 nmol/kg) immediately after the first training session failed to ameliorate learning ability in the CO-exposed group. These results suggest that (-)-nicotine potentiates the nicotinic cholinergic neuronal system and may potentiate acquisition of memory.

Amnesia↗
PubMed1989

Platelet aggregation in transient global amnesia.

We found a correlation between increased platelet aggregation parameters and transient global amnesia and no differences between patients with transient global amnesia and transient ischemic attacks. Our findings support the theory of a vascular mechanism for transient global amnesia.

Amnesia↗
PubMed2007

[Transient global amnesia (TGA) during an oral provocation test].

After the oral administration of the COX 2 inhibitor rofecoxib (Vioxx) as part of an oral provocation test, a 64-year-old woman developed acute anterograde and retrograde amnesia which lasted for several hours. The patient did not show symptoms of anaphylaxis. Neurological examination did not reveal focal symptoms or an epileptic seizure. Diffusion-weighted magnetic resonance imaging only showed a small region of increased signal intensity in the left hippocampus. The patient thus had no anaphylactic drug reaction, but a transient global amnesia (TGA) or amnestic episode. TGA is an acute, reversible, cerebral dysfunctional state which lasts from 1 h up to maximally 24 h and which is associated with anterograde and retrograde amnesia. While about half of the cases appear to occur spontaneously, other cases are preceded by physically or emotionally stressful events. In our patient it may have been the emotional distress caused by the oral provocation testing that has triggered the TGA. When TGA occurs during oral challenge of drugs, we recommend repeating the oral challenge of the tested drug.

Administration, Oral↗
PubMed2004

Metamemory without the memory: are people aware of midazolam-induced amnesia?

RATIONALE: Midazolam is a benzodiazepine which produces a dense anterograde amnesia, while permitting relatively well-preserved short-term memory, semantic retrieval, and other higher cognitive functions. Given these preserved abilities, we were interested in whether or not participants given midazolam would be aware of this anterograde amnesia. METHOD: In the present experiment, participants were given midazolam in one testing session and a saline placebo in another. Participants provided judgments-of-learning (JOLs) immediately following study of cue-target pairs. During the test phase of the experiment, confidence levels and feeling-of-knowing (FOK) judgments were collected. RESULTS: Although cued recall performance was substantially impaired in the midazolam condition, mean JOLs were unaffected, indicating participants had little insight into their impairment during the study phase. Participants were relatively accurate in confidence levels and FOK judgments in the midazolam condition. CONCLUSION: When studying items under the influence of midazolam, participants are unaware that their memory will be impaired. Implications for clinical practice and pharmacological studies of amnesia are discussed.

Adult↗
PubMed1993

Lack of the development of morphine tolerance in experimental amnesia: role of arginine vasopressin.

The development of tolerance to morphine analgesia in amnesic model mice and the role of arginine vasopressin (AVP) in the underlying mechanism was examined. Hypoxia, brain ischemia, scopolamine and electroconvulsive shock (ECS) manipulation caused amnesia in the step-through type passive avoidance learning test performed at 24 h after the training trial. The amnesic state lasted for at least 3 days and recovered to naive control level on the 20th day after each manipulation. In all amnesic groups, radioimmunoassayable AVP content in hypothalamus was decreased, in particular, the reduction was significant in hypoxia and ischemic induced amnesic animals, then recovered to the control level by 20 days after each treatment. Daily morphine, 10 mg/kg, s.c. easily resulted in the development of tolerance to the analgesic effect in control animals; however, such treatment failed to develop tolerance in amnesic model animals, leaving the analgesic effect unchanged to the control levels. Daily pretreatment with i.c.v. AVP, dose-dependently reinstated the development of tolerance in amnesic model mice. When morphine injection was started from 20 days after the amnesia inducing treatment, tolerance developed as in a similar pattern as in control animals. Thus, amnesic model mice are deficient in brain AVP levels, and consequently, a certain level of AVP in the hypothalamus is required for maintaining the normal function such as the development of tolerance to morphine and the recovery from amnesia.

Amnesia↗