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At least 19 recordsLinked to original sources
PubMed1983

Is anterograde amnesia a special case of retrograde amnesia?

In anterograde amnesia, memory loss is obtained for events that occur subsequent to the traumatic insult. But because the effects of an anterograde agent or treatment usually last for minutes, or even hours, after the nominal training event, processing of information may be altered during the postacquisition period as well as during acquisition. Since posttraining manipulations are themselves capable of modulating memory, or inducing retrograde amnesia, the memory loss due to a putative anterograde treatment may instead represent retrograde processes. The present experiment examined this potential source of confounding by using an amnestic treatment that can be quickly reversed after training in order to remove postacquisition effects. Thus, the presence of amnesia would isolate anterograde contributions as the source of loss. For induction of anterograde amnesia, rats were trained while at reduced body temperature (29 degrees C). A rapid rewarming procedure was introduced for some animals immediately after training to ensure that the hypothermic state did not extend into the postacquisition period. Other subjects were rapidly rewarmed 1 hr after training to control for any effects of the rewarming manipulation. Both groups showed severe anterograde amnesia that was indistinguishable from that obtained in the gradually rewarmed controls. These data provide an empirical example of an anterograde-induced memory deficit that is independent of retrograde influences.

Animals↗
PubMed1997

Massive and persistent anterograde amnesia in the absence of detectable brain damage: anterograde psychogenic amnesia or gross reduction in sustained effort?

The case of a young patient with severe and persistent anterograde amnesia of no known cause is reported. Anterograde amnesia arose within a 1-month period and has persisted for more than 1 year. Although a wide variety of neurological and neuroradiological assessments were completed (EEG, evoked potential recordings, Doppler sonography, MRI, PET), no evidence of brain damage was detected. Neuropsychologically, the patient was of high intelligence, had average to above-average short-term memory, and normal retrograde memory abilities, but severe and persistent anterograde amnesia in both verbal and nonverbal domains. Furthermore, he demonstrated grossly reduced long-term concentration. It is likely that a complex chain of interacting variables can produce a syndrome that appears phenomenologically as anterograde amnesia without organically measurable correlates.

Adult↗
PubMedDate not supplied

The relationships between temporal lobe and diencephalic structures implicated in anterograde amnesia.

The relationship between the anterograde amnesic syndromes associated with diencephalic and temporal lobe pathology is examined in the light of recent findings. It is proposed that a common feature of anterograde amnesia is damage to part of an "extended hippocampal system" comprising the hippocampus, the fornix, the mammillary bodies, and the anterior thalamic nuclei. Damage to this system results in deficits in the recall of episodic information, the core symptom of anterograde amnesia. In contrast, lesions in this system need not disrupt tests of recognition memory when they primarily tax familiarity judgements. It is assumed that familiarity judgements depend on other regions (e.g. the rhinal cortex in the case of temporal lobe amnesia) and that the extended hippocampal system is principally involved in those aspects of recognition that are retrieval-based rather than familiarity-based. These proposals arise from new evidence on the performance of delayed nonmatching-to-sample by animals, from a meta-analysis of the performance of amnesic subjects on a test of recognition memory, and from new research into the pattern of connections between the medial temporal lobe and the medial diencephalon in primates.

Amnesia↗
PubMed1997

The relationship between retrograde and anterograde amnesia in patients with typical global amnesia.

An extensive battery of tests of anterograde amnesia and remote memory was given to ten amnesics with lesions either to the medial temporal lobes of the diencephalon. These showed that the patients had anterograde amnesia with deficits in verbal and non-verbal recall and recognition, but preservation of word stem completion and intelligence. Mild impairments on executive tests and digit span performance were largely caused by the poor performance of the Korsakoff patients. The amnesics also showed remote memory deficits for personal and public domain information, and temporal gradients were observed for some of the tests. These deficits probably arose because the patients' anterograde amnesia was more severe than their retrograde amnesia even for the recent pre-morbid past. They were more impaired in the recall of details about famous names in their ability to recognize such names. There was also a suggestion that performance on anterograde tests did not relate strongly to that on tests of retrograde amnesia of the remote pre-morbid past. However, this effect was less apparent with memory for personal information when the format and the information tapped were matched on pre- and post-morbid tests.

Adult↗
PubMed1986

Korsakoff's syndrome: a study of the relation between anterograde amnesia and remote memory impairment.

Patients with Korsakoff's syndrome were evaluated with nine tests of new learning ability and three tests of remote memory to determine the correlation between anterograde amnesia and remote memory impairment. There was no correlation between the severity of anterograde amnesia and either the overall severity of remote memory impairment (1940s-1970s) or the impairment observed for more remote time periods (1940s-1950s). However, the correlation between remote memory impairment and anterograde amnesia became progressively stronger with the recency of the time period and was significant for the 1960s-1970s or the 1970s alone. The results support the view that the extensive remote memory impairment in Korsakoff's syndrome is, at least in part, distinct from and unrelated to anterograde amnesia. The more severe impairment observed for more recent time periods could be related to anterograde amnesia in that it reflects anterograde amnesia that was either already in place or progressively developing during recent years. The ability to recall very remote events seems therefore to depend on brain mechanisms distinct from those required for new learning or for recall of more recent events.

Alcohol Amnestic Disorder↗
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↗
PubMed2001

Study of cases of anterograde amnesia in a disease of mental disintegration.

Pierre Janet, in his famous paper (1892) on anterograde amnesia, is concerned with the theme of the disintegration of the human personality. He shows that the weakened personality may lose the power to assimilate memories of current events. After a severe shock, there may supervene not only a retrograde amnesia (a blotting out from memory from some period before the accident), but also a continued or anterograde amnesia, that is to say, an inability to remember events occurring after the accident. Janet details the circumstances of a very interesting case of amnesia resulting from an attack of hysteria, brought on by the shock of bad news. The patient, 'Mrs. D.', had wholly lost all memory of events that occurred during the month and a half before her attack, and since that time she had only been able to remember for a few moments what was going on around her. Janet shows that memories which appear not to be formed are in fact formed; that they exist somewhere in the patient's mind with the full vividness of ordinary recollections, and that they may spontaneously crop up in dreams, or may be called out by hypnotic suggestion, or by other methods.

Amnesia, Anterograde↗
PubMed1992

Anterograde amnesia in triazolam overdose despite flumazenil treatment: a case report.

Anterograde amnesia, possibly accompanied by acute brain syndrome, is a potential side-effect of certain benzodiazepines, particularly triazolam. Flumazenil is a benzodiazepine antagonist that is highly effective in reversing the central nervous system effects of benzodiazepine overdose. We report a case of triazolam overdose resulting in anterograde amnesia after flumazenil administration had restored clear consciousness. The defect in memory may have been due to too little flumazenil being given or failure of memory consolidation affected by the character of triazolam during the induced lucent period. We feel that physicians should be aware of the potential occurrence of acute brain syndrome in patients with benzodiazepine overdose despite treatment with flumazenil.

Adolescent↗
PubMed2001

The ventral hippocampus and fear conditioning in rats. Different anterograde amnesias of fear after tetrodotoxin inactivation and infusion of the GABA(A) agonist muscimol.

Studies on the involvement of the rat hippocampus in classical fear conditioning have focused mainly on the dorsal hippocampus and conditioning to a context. However, the ventral hippocampus has intimate connections with the amygdala and the nucleus accumbens, which are involved in classical fear conditioning to explicit and contextual cues. Consistently, a few recent lesion studies have indicated a role for the ventral hippocampus in classical fear conditioning to explicit and contextual cues. The present study examined whether neuronal activity within the ventral hippocampus is important for the formation of fear memory to explicit and contextual cues by classical fear conditioning. Tetrodotoxin (TTX; 10 ng/side), which completely blocks neuronal activity, or muscimol (1 microg/side), which increases GABA(A) receptor-mediated inhibition, were bilaterally infused into the ventral hippocampus of Wistar rats before the conditioning session of a classical fear-conditioning experiment. Conditioning to a tone and the context were assessed using freezing as a measure of conditioned fear. TTX blocked fear conditioning to both tone and context. Muscimol only blocked fear conditioning to the context. The data of the present study indicate that activity of neurons in the ventral hippocampus is necessary for the formation of fear memory to both explicit and contextual cues and that neurons in the ventral hippocampus that bear the GABA(A) receptor are important for the formation of fear conditioning to a context. In addition, both bilateral muscimol (0.5 microg/side and 1 microg/side) and TTX (5 ng/side and 10 ng/side) infusion into the ventral hippocampus dose-dependently decreased locomotor activity in an open-field experiment.

Acoustic Stimulation↗
PubMed2002

Interaction between midazolam-induced anterograde amnesia and memory enhancement by treatments given immediately after training on an inhibitory avoidance task in rats.

The aim of this study was to evaluate the effects of interactions between memory modulatory systems on inhibitory avoidance retention in rats. Adult female Wistar rats were trained and tested in a step-down inhibitory avoidance task (0.3 mA footshock). The training-test interval was 24 h. The animals received an intraperitoneal injection of saline or midazolam (1 mg/kg) 15 min before training, and saline, adrenaline (25 microg/kg), naloxone (0.4 mg/kg), dexamethasone (0.3 mg/kg) or glucose (320 mg/kg) immediately after training. In saline-pretreated rats, adrenaline, naloxone, dexamethasone and glucose enhanced memory retention. Pretreatment with midazolam prevented the facilitatory effects of those treatments. These findings suggest that the facilitation of learning by post-training memory-enhancing treatments is prevented by midazolam.

Amnesia, Anterograde↗
PubMed2006

MR imaging of human herpesvirus-6-associated encephalitis in 4 patients with anterograde amnesia after allogeneic hematopoietic stem-cell transplantation.

MR imaging is typically obtained during the work-up of patients who have undergone allogeneic hematopoietic stem-cell transplant who present with unexplained change in mental status, amnesia, or seizures. Although the differential diagnosis is broad in this setting, the presence of T2 prolongation limited to the medial aspect of one or both temporal lobes with or without associated reduced water diffusion may help limit the possible diagnoses. A frequent etiology seen in this context is human herpesvirus-6 (HHV6) infection. We report the evolution of MR imaging findings and clinical course in 4 patients with limbic encephalitis probably related to HHV6.

Adult↗