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PubMed1989

Effects of 5-HT2 receptor antagonist on cycloheximide-induced amnesia in mice.

A role played by serotonergic neuronal system in cycloheximide (CXM)-induced amnesia was studied in mice using a step-down passive avoidance task. CXM (30 mg/kg SC) given immediately after training caused impairment of memory. Nonselective serotonin (5-HT) antagonist methysergide and selective 5-HT2 antagonist ritanserin significantly attenuated impairment of memory caused by CXM. 5-HT1 antagonist (+/-)-pindolol had no effect on CXM-induced amnesia. The antiamnesic effect of ritanserin on CXM-induced amnesia was antagonized by 5-HT (ICV), but not by nonselective 5-HT agonist 5-methoxy-N,N-dimethyltryptamine and 5-HT1A selective agonist 8-hydroxy-2-(di-n-propylamino)tetralin at the dose level which did not cause the memory disruption. Scopolamine antagonized the antiamnesic effects of methysergide and ritanserin on CXM-induced amnesia. These results suggest that 5-HT2 receptors and cholinergic neuronal system may play an important role in memory formation.

Amnesia↗
PubMed1990

Effects of DM-9384, a pyrrolidone derivative, on alcohol- and chlordiazepoxide-induced amnesia in mice.

The effects of N-(2,6-dimethyl-phenyl)-2-(2-oxo-1-pyrrolidinyl) acetamide (DM-9384), a new pyrrolidone derivative, were investigated on ethanol- and chlordiazepoxide (CDP)-induced amnesia animal model using the passive avoidance task in comparison with aniracetam, another pyrrolidone derivative. Pretraining administration of DM-9384 attenuated ethanol- and CDP-induced amnesia, whereas aniracetam failed to do so. The effects of DM-9384 on CDP-induced amnesia were antagonized by bicuculline, a GABAA receptor antagonist, but not by scopolamine, a muscarinic acetylcholine receptor antagonist and flumazenil, a benzodiazepine receptor antagonist. These results suggest that DM-9384 attenuates CDP-induced amnesia by interacting with the GABAergic neuronal system.

Amnesia↗
PubMed1991

Naftidrofuryl oxalate, nootropic effects on the scopolamine- and the basal forebrain lesion-induced amnesia in rats.

We studied the effects of naftidrofuryl oxalate on scopolamine- and basal forebrain (BF) lesion-induced amnesia using passive avoidance and multiple T-maze tasks, in comparison with Ca-hopantenate and physostigmine in rats. In the passive avoidance task, one-week treatment with naftidrofuryl oxalate (12.5 and 25 mg/kg, IP) ameliorated BF lesion-induced amnesia. The multiple T-maze task was done with two training sessions per day for five continuous days. We measured the number of errors made from start box to goal box. Naftidrofuryl oxalate (12.5 mg/kg, IP, b.i.d.) and physostigmine (0.1 mg/kg, IP, b.i.d.) attenuated scopolamine- and BF lesion-induced amnesia. However, treatment with naftidrofuryl oxalate for one week failed to inhibit the decrease of the choline acetyltransferase induced by the BF lesion. Ca-hopantenate did not show attenuation of amnesia induced by the scopolamine or BF lesion. These results suggest that naftidrofuryl oxalate enhances the storage of spatial information, and that the nootropic effects of naftidrofuryl oxalate may be produced by an indirect activation of the cholinergic system through serotonergic neuronal systems.

Amnesia↗
PubMed1994

CGRP prevents electroconvulsive shock-induced amnesia in rats.

The effects of calcitonin gene-related peptide (CGRP) on electroconvulsive shock (ECS)-induced amnesia and the possible involvement of neurotransmitters in this action were studied in rats. ECS-induced amnesia was elicited in a passive avoidance paradigm. The possible roles of different transmitters involved in mediating CGRP action were followed by pretreating the animals with different receptor blockers in doses which themselves could not influence the paradigm. CGRP facilitated learning in the passive avoidance paradigm and prevented ECS-induced amnesia in a dose-dependent manner. Pretreatment with atropine, naloxone, phenoxybenzamine, or propranolol blocked the antiamnesic action of CGRP. Other receptor blockers, such as bicuculline, methysergide, and haloperidol, were ineffective. The results support our previous findings that CGRP facilitates passive avoidance learning and prevents ECS-induced amnesia. In the antiamnesic action of CGRP, cholinergic, opiate, and alpha- and beta-adrenergic mediators are involved.

Amnesia↗
PubMedDate not supplied

Detecting simulated amnesia for autobiographical and recently learned information using the P300 event-related potential.

To investigate whether the P300 (P3) event-related potential (ERP) can be used as an index of the intactness of recognition memory in subjects trying to simulate amnesia, two groups of subjects (n = 12 and n = 15) were instructed to simulate amnesia and one group of control subjects (n = 14) did not simulate amnesia while taking three recognition tests, during which ERPs were recorded. The three tests consisted of three different types of memory items: (1) the subject's birthday (birth), (2) the experimenter's name (name), (3) a word list of 14 nouns (words). The memory item was presented in a random series with other, similar in type, non-memory items. In group tests, memory items evoked larger amplitude P3s than non-memory items (p < 0.001). Within-subjects tests were used to determine whether the P3 amplitude in response to memory items was larger than the P3 amplitude in response to non-memory items for each individual. There was no difference between the sensitivity of the best within-subjects tests for amnesia simulators (birth = 0.9, name = 0.85, words = 0.53) versus non-simulators (birth = 1.0, name = 0.81, words = 0.5) averaged across the three test types. This suggests that P3 used as an index of the intactness of recognition memory may be useful in cases of suspected malingering.

Adult↗
PubMed1995

Acute confusional migraine: variant of transient global amnesia.

Acute confusional migraine in children and transient global amnesia in adults share a number of similar clinical manifestations. Acute confusional migraine in 6 children (mean age: 11.7 years; range: 7.5-17 years) was characterized by transient episodes of amnesia and acute confusion lasting 1-12 hours. Episodes were preceded by headache and vomiting in 4 patients. In 2 patients acute confusional migraine was the initial symptom. A history of preceding trivial head injury was reported in 3 patients and migraine in 4. Urine and serum drug screens were negative. Cerebral imaging studies and interictal electroencephalograms were normal. Ictal electroencephalograms in 3 patients revealed diffuse or bioccipital delta wave slowing. Recurrent episodes of acute confusional migraine occurred in 2 children during 1-3 years of follow-up. The clinical manifestations of acute confusional migraine in this series of children are similar to those reported in transient global amnesia. The similarity of the clinical manifestations of acute confusional migraine in children and transient global amnesia in adults suggests that these disorders may share a common pathophysiology.

Acute Disease↗
PubMed2004

Symptom validity testing of feigned amnesia for a mock crime.

Perpetrators sometimes claim loss of memory for the crimes they have committed. For the neuropsychologist, the veracity of such crime-related amnesia is difficult to assess. The aim of the present study was to investigate whether Symptom Validity Testing (SVT) can be used to detect feigning of crime-related amnesia. Undergraduate students (N = 39) were instructed to commit a mock crime and asked to feign complete amnesia for the event. Subsequently, they were given 25 forced-choice items about the "crime" that were always followed by the correct answer and an equally plausible alternative. To counteract chance performance, test items were intermixed with 25 bogus questions that contained two equally plausible alternatives. Results show that a majority of participants (59%) scored below chance level on the critical items of the SVT. In addition, debriefing interviews showed that understanding the rationale behind the SVT was not related to chance performance. SVT procedures therefore might be helpful in identifying feigned crime-related amnesia.

Adolescent↗
PubMed2004

Procedural memory in dissociative identity disorder: when can inter-identity amnesia be truly established?

In a serial reaction time task, procedural memory was examined in Dissociative Identity Disorder (DID). Thirty-one DID patients were tested for inter-identity transfer of procedural learning and their memory performance was compared with 25 normal controls and 25 controls instructed to simulate DID. Results of patients seemed to indicate a pattern of inter-identity amnesia. Simulators, however, were able to mimic a pattern of inter-identity amnesia, rendering the results of patients impossible to interpret as either a pattern of amnesia or a pattern of simulation. It is argued that studies not including DID-simulators or simulation-free memory tasks, should not be taken as evidence for (or against) amnesia in DID.

Amnesia↗
PubMed2004

Effects of baicalein on beta-amyloid peptide-(25-35)-induced amnesia in mice.

Baicalein may act on the benzodiazepine binding sites to exert an anxiolytic-like effect in mice. Since many benzodiazepine drugs have amnesic side-effect and baicalein can protect cultured cortical neurons from beta-amyloid peptide-(25-35)-induced toxicity, this study examined the amnesic effect of baicalein and its effects on beta-amyloid peptide-(25-35) (3 nmol/mouse, i.c.v.)-induced amnesia in mice. Using the step-through passive avoidance test, the results showed that baicalein (10-100 mg/kg, i.p.), unlike the benzodiazepine drug chlordiazepoxide (10 mg/kg, i.p.), had no significant amnesic effect. Baicalein (10-50 mg/kg, i.p.) also had no facilitating effect on the learning and memory. However, one dosage pretreatment, but not post-treatment, of baicalein (5 or 10 mg/kg, i.p.) attenuated beta-amyloid peptide-(25-35)-induced amnesia. Interestingly, post-treatment for 7 or 13 days of baicalein (10-15 mg/kg/day, i.p.), like melatonin (10 mg/kg/day, i.p.), also attenuated beta-amyloid peptide-(25-35)-induced amnesia. Therefore, this study demonstrated that baicalein has protective effect on beta-amyloid peptide-(25-35)-induced amnesia.

Amnesia↗
PubMed2006

Conditional discrimination and reversal in amnesia subsequent to hypoxic brain injury or anterior communicating artery aneurysm rupture.

Human anterograde amnesia can develop following bilateral damage to the hippocampus and medial temporal lobes, as in hypoxic brain injury, or following damage to the basal forebrain, as following anterior communicating artery (ACoA) aneurysm rupture. In both cases, the mnestic deficit may be similar when assessed by standard neuropsychological measures. However, animal and computational models suggest that there are qualitative differences in the pattern of impaired and spared memory abilities following damage to hippocampus versus basal forebrain. Here, we show such a dissociation in human amnesia using a single two-stage task, involving conditional discrimination and reversal. Consistent with a prior study, 10 individuals with anterograde amnesia subsequent to hypoxic brain injury were spared on acquisition but impaired at reversal. However, 10 individuals with amnesia subsequent to ACoA aneurysm showed the opposite pattern of impaired acquisition but spared reversal. The differences between groups cannot be easily ascribed to severity of mnestic or cognitive deficit, since the two amnesic groups performed similarly on neuropsychological tests of memory, intelligence and attention. The results illustrate qualitative differences in memory impairments in hypoxic and ACoA amnesics and highlight the importance of considering etiology in evaluating mnemonic deficits in amnesic populations.

Adult↗
PubMed2005

Increasing the salience of fluency cues reduces the recognition memory impairment in amnesia.

The present study examined whether the recognition memory deficit in amnesia would be attenuated under conditions that increased the salience of study-induced fluency. Studied and unstudied items were drawn either from separate pools of letters (no-overlap condition) or from the same pool of letters (overlap condition). Study-induced fluency was more salient in the no-overlap than in the overlap condition, because in the no-overlap condition, such fluency occurred at the letter level as well as at the word level. The recognition memory impairment in amnesia was smaller in the no-overlap than in the overlap condition. These findings are consistent with the idea that enhancing the salience of fluency cues promotes reliance on a fluency heuristic that ordinarily is not fully engaged in amnesia, and reduces the recognition memory impairment in amnesia.

Amnesia↗
PubMed2004

Effects of steroid hormones on (Na+, K+)-ATPase activity inhibition-induced amnesia on the step-through passive avoidance task in gonadectomized mice.

Inhibition of sodium-potassium adenosine 5'-triphosphatase ((Na(+), K(+))-ATPase) activity causes edema and cell death in the central nervous system, and impairment of learning and memory. Several sex steroid hormones have a protective effect against neuronal cell damage and the hypofunction of learning and memory. To examine the possible roles and mechanism of action of steroid hormones against amnesia induced by ouabain, an inhibitor of (Na(+), K(+))-ATPase, gonadectomized male mice were administrated ouabain (0.1 microg per mouse) intracisternally (i.cist.), and the learning and memory abilities of the mice were assessed by a step-through passive avoidance task. Subcutaneous (s.c.) administration of 17beta-estradiol (betaE2; 10 microg kg(-1)) or testosterone (TES; 1 mg kg(-1)) improved the memory impairment induced by ouabain, while administration of dihydrotestosterone (1 mg kg(-1)) or corticosterone (COR) (1 mg kg(-1)) did not. Treatment with the estradiol receptor antagonists, tamoxifen (TAM) (10 mg kg(-1); s.c. or 0.1 microg; i.cist.) and 4-hydroxytamoxifen (10 mg kg(-1); s.c.), or the androgen receptor antagonist, cyproterone (10 mg kg(-1); s.c. or 1 microg; i.cist.), did not influence the protective effect of betaE2 or TES on ouabain-induced amnesia. Moreover, we studied the effects of several free radical scavengers-17alpha-estradiol (10 microg kg(-1); s.c.), alpha-tocopherol (VE: 200 mg kg(-1); per os (p.o.), ascorbic acid (VC: 200 mg kg(-1); p.o.), or VE+VC (200 mg kg(-1) each; p.o.)-on ouabain-induced amnesia, and compared those effects with that of betaE2. The administration of free radical scavengers had no significant effect on memory impairment. These results indicate that betaE2 and TES ameliorate the amnesia induced by inhibition of (Na(+), K(+))-ATPase activity, and that the protective effect of betaE2 is caused by a non-genomic, rather than a genomic effect or a radical scavenging action. Additionally, the ameliorative effect of TES does not appear to involve free radical scavenging, but its aromatization to estrogen could contribute to the non-genomic action of betaE2.

Amnesia↗
PubMed2006

Influence of nitric oxide on morphine-induced amnesia and interactions with dopaminergic receptor agents.

The interactions of dopaminergic receptors and nitric oxide (NO) with morphine-induced memory of passive avoidance have been investigated in mice. Pre-training administration of morphine (1, 3 and 5 mg/kg, s.c.) dose-dependently decreased the learning of a one-trial passive avoidance task. Pre-training administration of L-arginine, a nitric oxide precursor (50, 100 and 200 mg/kg, i.p.), alone did not affect memory formation. The drug (100 and 200 mg/kg) decreased significantly amnesia induced by pre-training morphine (5 mg/kg). Pre-training administration of L-NAME (N(G)-nitro-L-arginine methyl ester), a nitric oxide synthase (NOS) inhibitor (20 and 30 mg/kg, i.p.), dose-dependently impaired memory formation. In addition, co-pretreatment of different doses of L-NAME (10, 20 and 30 mg/kg) with lower dose of morphine (1 mg/kg), which did not induce amnesia by itself, caused inhibition of memory formation. Pre-training administration of apomorphine, a dopaminergic receptor agonist (0.25, 0.5 and 1 mg/kg, i.p.), alone also did not affect memory formation, but morphine-induced amnesia was significantly inhibited by pretreatment with apomorphine (0.5 and 1 mg/kg, 5 min, i.p.). On the other hand, the inhibition of morphine-induced amnesia by L-arginine (200 mg/kg, i.p.) was significantly decreased by pretreatment with different doses of dopamine D1 receptor antagonist, SCH 23390 (0.001, 0.01 and 0.1 mg/kg, i.p.) or D2 receptor antagonist, sulpiride (12.5, 25, 50 and 100 mg/kg, i.p.). However, the dopamine receptor antagonists could not affect memory formation by themselves. It may be concluded that the morphine-induced impairment of memory formation can be prevented by nitric oxide donor and, in this effect, dopaminergic mechanism is involved.

Amnesia↗
PubMed2004

Clinically relevant anterograde amnesia and its relationship with blood levels of benzodiazepines in suicide attempters who took an overdose.

The relationship between anterograde amnesia, sedation and plasma levels of benzodiazepines was studied prospectively in a group of 24 patients who took an overdose of benzodiazepines. Patients were tested on two sequential days after having taken an overdose. Anterograde amnesia was tested by using a verbal recall test and a photo recognition test. Sedation was scored on a visual analogue scale (VAS) by the patient and the interviewer. The concentration of benzodiazepines in plasma was measured by using a radioreceptor assay that adds benzodiazepines and their active metabolites. The cumulative amount of benzodiazepines was expressed as diazepam equivalents (DZE). Diazepam equivalents determined by this radioreceptor assay were significantly higher on the first day than on the second day. Ratings on the verbal recall test were significantly lower on the first day than on the second day. There was a significant relation between decrease of diazepam equivalents and increase of verbal recall: more than 30% of increase of verbal recall was explained by decrease of diazepam equivalents. There was not a strong relation between decrease of diazepam equivalents and reduction of level of sedation as scored by the patients. There was almost no relation between decrease of diazepam equivalents and reduction of level of sedation as scored by the interviewer. No relation was found between verbal recall, sedation and diazepam equivalents. There was no relation between diazepam equivalents and photo recognition. It was concluded that anterograde amnesia was strongly associated with benzodiazepines in patients who take benzodiazepines in an overdose. Sedation does not predict the degree of anterograde amnesia.

Adult↗
PubMed2000

Profound retrograde amnesia following mild head injury: organic or functional?

This paper describes a 56 year old female patient (JJ) who suffered a minor head injury at work and presented with profound retrograde amnesia for both public events and autobiographical material spanning her entire life. In addition, she complained of word-finding difficulties and anterograde memory impairment and neuropsychological assessment found evidence of mild executive dysfunction. Neurological investigations (CT and EEG) were essentially normal although changes indicative of small vessel disease were noted on MRI brain scan. Various forms and aetiologies of remote memory loss were considered including, simulated, psychogenic and organic amnesia, but differential diagnosis proved difficult. It is proposed that criteria used in clinical practice to differentiate functional and organic complaints are limited and this may be because (1) both factors can be involved in the aetiology of amnesia, and (2) a similar underlying brain mechanism, such as a retrieval deficit could underlie many instances of organic and psychogenic amnesia. Future research, complemented by functional brain imaging, is needed to explore the nature of retrieval deficits.

Amnesia, Retrograde↗
PubMed1981

Transient global amnesia associated with bradycardia and temporal lobe spikes.

This paper presents electroencephalographic evidence of bilateral independent temporal lobe spiking during an episode of transient global amnesia. The amnesia occurred during a period of hypotension secondary to sinus bradycardia. The amnesia recurred in absence of bradycardia and hypotension. The temporal lobe spiking leads credence to the thought that transient global amnesia occurs as the result of seizure activity.

Aged↗
PubMed1997

Is memory loss without anatomical damage tantamount to a psychogenic deficit? The case of pure retrograde amnesia.

Following a car accident, a patient remained unconscious for approximately 20 min and confused for a few hours. When he could be questioned, he was found to have lost all past memories. The retrograde amnesia covered his whole life and concerned autobiographic events as well as famous facts and encyclopaedic knowledge. It also partially involved the verbal and visual lexicon. Reading, writing and counting were no longer possible. The profound impairment of retrograde memory contrasted with the preservation of anterograde memory, which permitted the patient to reacquire some of the notions he had lost, without, however, recovering the feeling of a personal experience of autobiographical information. Four years later, the retrograde deficit was unmodified, except for what had been relearnt. The search for data in support of an organic or psychological aetiology was negative. No signs of brain damage were apparent at the neurological examination and on CT, MRI and SPECT. On the other hand, there was no evidence of a psychiatric history, psychological stress or emotional precipitants that could substantiate the hypothesis that the patient derived a primary or secondary gain from amnesia. We propose that cases of focal retrograde amnesia, similar to the present one, deserve to be classified separately from organic and psychogenic forms under the label of 'functional' retrograde amnesia, a syndrome in which the threshold of activation of premorbid memories is abnormally raised by the trauma, leaving the encoding and retrieval of new memories unaffected.

Agraphia↗
PubMed1997

Severe amnesia: an usual late complication after temporal lobectomy.

A patient developed the severe amnesic syndrome 8 years after temporal lobe surgery for epilepsy. He underwent left temporal lobectomy (6 cm, 43.5 g; hippocampal sclerosis) aged 19, and remained seizure free for 8 years until a convulsion followed a head injury. He became severely amnesic after a fourth convulsion 16 months later. He was right-handed, pre-operative IQ was average, verbal memory poor and non-verbal memory normal. Post-operatively, these were unchanged. After the first post-operative seizure he began professional training. After onset of amnesia IQ was unchanged, anterograde memory severely impaired and retrograde amnesia dense for at least 16 months. He died 2 years later. Magnetic resonance imaging before amnesia showed absence of anterior left temporal lobe, atrophy of left fornix and mamillary body, and normal right temporal lobe. Four months after onset of amnesia, right hippocampal volume had reduced by 36%. Autopsy showed: previous left temporal lobectomy with absence of left amygdala and hippocampus, atrophy of fornix and mamillary body; neuronal loss in the right hippocampus, severe in CA1 and CA4; intact right amygdala and parahippocampal gyrus; recent diffuse damage associated with cause of death. A convulsion can cause severe hippocampal damage in adult life. Hippocampal zones CA1 and/or CA4 are critical for maintaining memory and the amygdala and parahippocampal gyrus cortex alone cannot support acquisition of new memories.

Adult↗