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PubMed1998

Apparent amnesia on experimental memory tests in dissociative identity disorder: an exploratory study.

Dissociative identity disorder (DID; called multiple personality disorder in DSMIII-R) is a psychiatric condition in which two or more identity states recurrently take control of the person's behavior. A characteristic feature of DID is the occurrence of apparently severe amnestic symptoms. This paper is concerned with experimental research of memory function in DID and focuses on between-identity transfer of newly learned neutral material. Previous studies on this subject are reviewed and a pilot study with four subjects is described. This study is specifically concerned with the question whether self-reported asymmetries in between-identity transfer can be replicated on experimental memory tests. A secondary aim was to examine whether, in the absence of explicit transfer, implicit transfer of information would occur. The results showed that the apparent amnestic asymmetry for explicit information was substantiated in the laboratory, although at least some leakage was present between the apparently amnestic identities. No evidence was found for better performance on implicit than on explicit memory tests in the apparently amnestic identities. In the discussion, parallels between apparent amnesia in DID and state-dependent memory are drawn, and the question of simulated amnesia is addressed.

Adult↗

PubMed1995

Two time windows of anisomycin-induced amnesia for passive avoidance training in the day-old chick.

The antibiotic anisomycin (ANI), a protein synthesis inhibitor, was used to investigate the time-related changes in protein synthesis following passive avoidance training in the day-old chick. Retention of memory for this simple learning task is known to be prevented by protein synthesis inhibitors within the first hour post-training. Here we report a second, later time window during which inhibition of protein synthesis results in amnesia following one-trial passive avoidance training. Birds were given bilateral intracranial injections of ANI (10 microliters/hemisphere of a 30 mM solution) at various times relative to training and tested 24 h later. Injections given between 0.5 h prior to 1.5 h post-training or 4-5 h post-training, but not at later or at intervening times, resulted in amnesia. These results are discussed in the context of earlier findings, using the inhibitor of glycoprotein synthesis 2-deoxygalactose, that memory formation shows two glycoprotein-synthesis-dependent periods of sensitivity (Scholey, Rose, Zamani, Bock, & Schachner, 1993). The time windows of susceptibility of ANI and 2-Dgal are consistent with a model in which there are two waves of neural activity following training; during the second, commencing 4 h after training, proteins are synthesized and then glycosylated as part of the establishment of an enduring memory trace.

Amnesia↗

PubMed1990

The novel anticonvulsant loreclezole (R 72063) does not produce diazepam-like anterograde amnesia in a passive avoidance test in rats.

Rats were injected intraperitoneally with loreclezole (R 72063), diazepam, or scopolamine 60 min prior to acquisition of a passive avoidance task and tested 18 h later for retention of the learned (passive) behavior. The known impairment of performance produced by diazepam in this test is believed to be a model for the clinically observed diazepam-induced anterograde amnesia in humans. We report in this study that (1) consistent with the literature, pretreatment with diazepam (2.0-16.0 mg/kg i.p.) or scopolamine (3.0 mg/kg i.p.) produced impairment in passive avoidance performance of rats (anterograde amnesia), but (2) pretreatment with loreclezole (R 72063) (2.0-80.0 mg/kg i.p.) did not impair the acquisition, retention, or the retrieval (tested 18 h later) of passive avoidance behavior by rats at any dose. The results suggest that the anticonvulsant activity of loreclezole is mediated by a mechanism distinct from the one coupled to diazepam-like disruption of cognitive functions involved in the acquisition or posttraining information processing of passive avoidance behavior.

Amnesia↗

PubMed1988

Attenuation of scopolamine-induced amnesia in mice.

Numerous studies suggest that age-related declines in memory storage are related to impairment of central cholinergic systems. Scopolamine, a muscarinic cholinergic antagonist, has been used with young humans and other animal species as a model of the cognitive impairment that often accompanies normal and pathological aging. The present study examined whether amnesia induced by scopolamine could be counteracted in mice by arecoline, a cholinergic agonist, or by other drugs, epinephrine or glucose, which have been found to enhance memory in aged rodents and humans. Young mice were administered scopolamine (3 mg/kg, IP) or saline prior to training on an inhibitory avoidance apparatus. Immediately after training, animals received injections of epinephrine (0.01, 0.05, 0.1, and 0.2 mg/kg), glucose (10, 100, and 250 mg/kg), arecoline (0.5, 1, 2, 5, 10, and 20 mg/kg), or saline. The results indicate that pre-training scopolamine reliably impaired retention assessed in test trials 48 h after training. This impairment was not attenuated by any post-training dose of arecoline; however, immediate post-training injections of both epinephrine (at 0.05 mg/kg) and glucose (at 100 mg/kg) significantly reduced the amnesia. Neither of these drugs was effective if injections were delayed by 1 h after training. These results support the value of scopolamine as a model of age-related memory impairments, but suggest further that these memory deficits may be particularly susceptible to attenuation with non-cholinergic treatments.

Aging↗

PubMed1983

Transient global amnesia as a manifestation of Epstein-Barr virus encephalitis.

A 43-year-old man developed severe global amnesia with uncinate fits and a single generalised convulsion 10 days after a febrile infection. CSF pleocytosis and serological findings indicated an acute Epstein-Barr virus encephalitis. All of the symptoms cleared within 2 weeks except for occasional generalised seizures. This seems to be the first observation of Epstein-Barr virus encephalitis presenting predominantly as transient global amnesia.

Adult↗

PubMed1981

Qualitative analysis of scopolamine-induced amnesia.

The neurochemistry of memory remains to be determined. Acetylcholine may be one of the neuotransmitters which mediates memory function, since the anticholinergic drug scopolamine produces amnesia in man. This study of scopolamine-induced memory deficits further defines those cognitive processes which are disrupted. The drug does not diminish attention, as assessed with an auditory vigilance task, or initial signal detection. More complex auditory decoding is affected, however. Scopolamine impairs aspects of initial memory acquisition (e. g., encoding and consolidation) and spontaneous memory retrieval. Retention is unaffected. Precise delineation of the neurochemistry of human memory will require comparative studies of amnesia-producing compounds, systematically examining the neuropsychological processes impaired by each.

Adult↗

PubMed1981

Effects of 4-hydroxy, 4-phenyl, caproamide on pentylenetetrazol-induced amnesia.

Early reports suggest a relationship between pentylenetetrazol-induced convulsions (PTZ) and amnesia. 4,-Hydroxy,4-phenyl caproamide (YPCA) is potently anti-convulsant against PTZ-induced convulsions. The purpose of these experiments is to show the possible role of PTZ in these amnestic effects. Experiment 1 proves YPCA antagonism of PTZ-induced convulsions in mice. Experiment 2 shows how YPCA, injected before PTZ and after animal training, protects against convulsions, leaving memory storage unaffected. However, when YPCA is injected before training (10 and 5 min) and PTZ 15 min afterwards (5 and 10 min after training), a retention impairment was observed. The results are discussed in terms that emphasize the need of convulsions in retrograde amnesia. Experiment 3 shows that foot shock is necessary for passive avoidance acquisition. Experiment 4 shows that subconvulsive doses of PTZ (5,10,20, and 40 mg/kg-1) have no effect on memory.

Amides↗

PubMed1981

Testing cyclic AMP mediation of memory: reversal of alpha-methyl-p-tyrosine-induced amnesia.

Treatments that increased intracellular cyclic 3',5' adenosine monophosphate (cAMP) levels following catecholamine depletion caused by alpha-methyl-p-tyrosine (AMPT) provided a prophylactic effect against AMPT-induced amnesia. This effect gives evidence that cAMP mediated the formation of memory. In Experiment I, the phosphodiesterase inhibitor papaverine (50 mg/kg), immediately after a one-trial acquisition task, functionally increased cAMP levels and prevented amnesia 3 h after treatment with AMPT (200 mg/kg) for New Zealand A strain (NZ/A) mice tested in a step-through passive avoidance apparatus. Retention test latencies 72 h later were significantly higher for animals that received only saline and for animals that received AMPT and papaverine than for animals that received AMPT and saline (the amnesic group). In a similar task (Experiment II), mice that received an intracerebroventricular injection of either 5 or 10 microgram dibutyryl cAMP immediately after acquisition and 3 h after AMPT administration showed significantly higher retention test latencies than animals that received AMPT and saline. The AMP plus 10 microgram dibutyryl cAMP group showed facilitated performance even compared to the saline plus saline group.

Amnesia↗

PubMed1992

Transient global amnesia after cerebral angiography with iohexol.

We describe a patient without a previous history of migraine or epilepsy and with no known vascular risk factors, who suffered subarachnoid haemorrhage. During vertebral angiography using nonionic contrast medium (iohexol), spasm of the basilar artery was seen. The patient suffered transient global amnesia. Angiography 3 months later with the same contrast medium was normal and produced no further deficit. This case lends support to the supposed ischaemic aetiology of transient global amnesia; in patients without other evidence of cerebrovascular disease, arterial spasm may be responsible.

Amnesia, Retrograde↗

PubMedDate not supplied

The role of GABAA and GABAB receptors in the development of amnesia.

It has been demonstrated that a gradual spontaneous recovery of a previously unreproducible memory trace and the prevention of the antiamnesic effect of the blockade of the GABAA receptor, but not of the blockade of the benzodiazepine receptor or the chloride channel, take place with the development of amnesia against the background of the activation of the GABAB receptor by baclofen. The "neurochemical set" created by the activation of the GABAA receptor by muscimol in a dose of 1 mg/kg prevents the antiamnesic effect of the blockade of any component of the benzodiazepine-GABA-ionophore complex, while at a dose of muscimol of 0.5 mg/kg, the retrieval of the amnestic trace takes place only by blockade of the benzodiazepine receptor. Thus, the development of amnesia is determined by the functional state of inhibitory GABAergic systems of the brain, which governs the subsequent correction of the amnestic memory trace.

Amnesia↗

PubMed1997

Transient procedural amnesia.

A man experienced temporary amnesia for tasks which he was used to performing daily as they were the core of his working activity (bread making). No overt etiology was found. We hypothesized a disorder that is similar to transient global amnesia, but selectively affects procedural memory.

Amnesia↗

PubMed1986

Neuropsychological findings during a transient global amnesia attack and its follow-up.

An extensive neuropsychological study was made during an attack of transient global amnesia and during four follow-up. The neuropsychological findings are compared to those of previous reports. Transient global amnesia appears to be a relatively benign syndrome but it leaves some "fragility" of memory, detected by complex neuropsychological tasks.

Amnesia↗

PubMed1992

Transient topographical amnesia.

A woman experienced three isolated episodes of loss of topographical memory, without overt etiology. A rare form of selective non verbal transient amnesia, similar to the more common transient global amnesia, is postulated.

Amnesia↗

PubMed1993

Effects of acute doses of oxiracetam in the scopolamine model of human amnesia.

The scopolamine model of amnesia has been used to test the pharmacodynamic efficacy of oxiracetam in 12 healthy volunteers. The subjects were divided into four experimental groups, according to a double-blind cross over incomplete randomized block design. After a baseline neuropsychological examination, each subject received in two separate sessions one of the following treatments, as acute oral doses: oxiracetam 800, 1600, 2400 mg or placebo. One hour after treatment scopolamine hydrobromide (0.5 mg) was given subcutaneously. The cognitive performance was tested before and 1, 2, 3 and 25 h after scopolamine administration. Scopolamine caused a deterioration of performance of verbal episodic memory, semantic memory and attention tests. In comparison to placebo, oxiracetam improved the overall test performance, with a statistically significant difference at the dose of 1600 mg on delayed recall of word lists, and showed dose-related antagonism of scopolamine-induced effects also on semantic memory and attention. The efficacy of an acute dose of oxiracetam in reducing scopolamine-induced cognitive impairment supports the potential usefulness of this pharmacological model of amnesia for studying the effects of cognition enhancers in humans.

Adult↗

PubMedDate not supplied

Recovery of memory in chicks after disruption during learning: the reversibility of amnesia induced by protein synthesis inhibitors.

Protein synthesis inhibitors given during learning are known to disrupt memory in various animal species in several models of learning. However, there are suggestions that amnesia induced by protein synthesis inhibitors is not permanent--memory can be recovered by a reminder procedure, i.e., by presenting the animal with one of the components of the external environment which was part of the learning situation. The aim of the present work was to determine the existence of the reminder phenomenon in a well-studied model of single-session training to passive avoidance in chicks. Cycloheximide and anisomycin were used to induce amnesia. Reminder was performed using the aversive taste of methylanthranilate 24 h after training, and testing was conducted 48 h after training. The results obtained provide evidence that memory disrupted by protein synthesis inhibitors in chicks can be recovered by the reminder procedure.

Amnesia↗

PubMed1998

Effect of pertussis toxin on baclofen- and diphenhydramine-induced amnesia.

The effect of pretreatment with pertussis toxin at the doses of 0.25 and 0.50 microg per mouse ICV on the amnesic effect produced by baclofen (0.1 4 mg kg(-1) i.p.), diphenhydramine (15-30 mg kg(-1) i.p.) and scopolamine (0.5-5 mg kg(-1) i.p.) was investigated in the mouse passive avoidance test. Ten days after a single injection of pertussis toxin, baclofen (2 4 mg kg(-1) i.p.) amnesia was prevented. By contrast, pertussis toxin had no effect on diphenhydramine- and scopolamine-induced amnesia. Pretreatment with pertussis toxin at both doses used did not impair motor coordination of the mice, as revealed by the rota-rod test. The present results indicate that the activation of pertussis toxin-sensitive G-proteins represents an important transduction step in memory impairment induced by GABA(B) (gamma-aminobutyric acid B) agonists, but not by antihistaminic and antimuscarinic drugs.

Amnesia↗

PubMed1999

Effects of chlordiazepoxide and FG 7142 on a rat model of diencephalic amnesia as measured by delayed-matching-to-sample performance.

The intralaminar thalamic nuclei (ILn) have been implicated as a critical site of pathology in amnesia. Lesions of the ILn have been found to produce behavioral effects comparable to benzodiazepine (BDZ) receptor agonists. We compared the effects of chlordiazepoxide (CDP), a BDZ agonist, and FG 7142, a partial inverse agonist at the BDZ receptor, in rats with thalamic lesions and in unlesioned controls. Delayed matching-to sample (DMS) performances were studied during treatment with ascending doses of CDP, counterbalanced trials with 2.5 mg/kg CDP and saline, ascending doses of FG 7142, and (for unlesioned controls only) counterbalanced trials with saline and higher doses of CDP. CDP had effects similar to the ILn lesion, decreasing response speed and percent correct responding in a delay-independent fashion. These effects were additive with the impairments associated with the ILn lesion. The effects of FG 7142 were more complex. At lower doses, it increased response speed without affecting response accuracy. At higher doses, it diminished both the speed and the accuracy of DMS responding. These results support the hypothesis that ILn lesions and BDZ agonists have similar effects on DMS performance. The biphasic effects observed for FG 7142 are consistent with other evidence that low doses of this drug enhance while higher doses impair memory performance. Although DMS accuracy was not improved, the enhancement observed for response speed provides evidence that partial inverse BDZ agonists have potential utility as treatments for cognitive impairments associated with amnesia.

Amnesia↗

PubMed2004

Is transient global amnesia a risk factor for amnestic mild cognitive impairment?

Transient Global Amnesia (TGA) is a common condition of unknown aetiology characterised by the abrupt onset of severe anterograde amnesia, which lasts less than 24 hours. Some authors have suggested that subclinical impairment of memory functions may persist for much longer, but neuropsychological assessment lasting years after TGA attack has not been performed so far. The aim of this study was to evaluate longterm cognitive functions in patients with a previous TGA episode. Fifty-five patients underwent a standardised neuropsychological assessment after at least one-year from the TGA attack, and were compared with 80 age-matched controls. TGA patients showed worse performances on tests evaluating verbal and nonverbal long-term memory and attention, with comparable global cognitive functions. By applying current criteria for amnestic Mild Cognitive Impairment (MCI-a) on TGA subjects, a group consisting of 18/55 (32.7%) MCI-a subjects was identified. There was no association between the presence of MCI-a and demographic variables, vascular risk factors, years since the TGA episode, or ApoE genotype. This study demonstrates that TGA appears to be a relatively benign syndrome although objective memory deficits fulfilling MCI-a criteria persist over time, as detected by multidimensional neuropsychological tasks performed at long-term follow-up.

Aged↗