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PubMed1986

[Plasma concentration and amnesia following lormetazepam and flunitrazepam in i.v. premedication].

The correlation between serum levels and degree of amnesia following 0.03 mg/kg lormetazepam or 0.02 mg/kg flunitrazepam was analysed in a prospective randomised single-blind study evaluating 20 patients with ASA classification I in each group. Blood specimens were drawn and amnesia tests performed 20, 40 and 60 min. after drug administration. The plasma level of lormetazepam was 1.8 to 2.0 times higher than that of flunitrazepam; however, the difference of lormetazepam concentrations was considerably large between the investigated individuals. There was no difference in the degree of amnesia, but also no correlation with plasma levels was measured. A serum level breakpoint for the occurrence of amnesia could not be defined.

Adolescent↗
PubMed1995

Memory and psychoanalysis: a new look at infantile amnesia and transference.

OBJECTIVE: This article reexamines the psychoanalytic concepts of infantile amnesia and transference in the light of certain findings derived from neurobiological research, information-processing theory, child development research, cognitive-developmental theory, and, more speculatively, evolutionary theory concerning memory. METHOD: Relevant developments from recent research in the neurosciences, and psychopathological phenomena in two psychiatric disorders--posttraumatic stress disorder and child abuse--in which memory changes are of critical importance, are first reviewed briefly. Four alternative hypotheses for infantile amnesia and three for transference are then derived from this review. RESULTS: The hypotheses discussed provide plausible alternative explanations for at least part of the phenomena classically subsumed in the psychoanalytic concepts of infantile amnesia and transference. CONCLUSIONS: Neurobiological, information-processing, developmental shifts, cognitive-developmental, and evolutionary findings and theories provide alternative hypotheses for infantile amnesia and transference that suggest a need for revisions and redefinitions for these two psychoanalytic concepts.

Child↗
PubMed2006

Hippocampal contributions to recollection in retrograde and anterograde amnesia.

Lesions restricted to the hippocampal formation and/or extended hippocampal system (hippocampal formation, fornix, mammillary bodies, and anterior thalamic nuclei) can disrupt conscious recollection in anterograde amnesia, while leaving familiarity-based memory relatively intact. Familiarity may be supported by extra-hippocampal medial temporal lobe (MTL) structures. Within-task dissociations in recognition memory best exemplify this distinction in anterograde amnesia. The authors report for the first time comparable dissociations within recognition memory in retrograde amnesia. An amnesic patient (A.D.) with bilateral fornix and septal nuclei lesions failed to recognize details pertaining to personal past events only when recollection was required, during recognition of episodic details. His intact recognition of generic and semantic details pertaining to the same events was ascribed to intact familiarity processes. Recollective processes in the controls were reflected by asymmetrical Receiver's Operating Characteristic curves, whereas the patient's Receiver's Operating Characteristic was symmetrical, suggesting that his inferior recognition performance on episodic details was reliant on familiarity processes. Anterograde and retrograde memories were equally affected, with no temporal gradient for retrograde memories. By comparison, another amnesic person (K.C.) with extensive MTL damage (involving extra-hippocampal MTL structures in addition to hippocampal and fornix lesions) had very poor recognition and no recollection of either episodic or generic/semantic details. These data suggest that the extended hippocampal system is required to support recollection for both anterograde and retrograde memories, regardless of their age.

Age Factors↗
PubMed1976

[Clinical observations on the psychopathology of amnesic episodes (transient global amnesia) (author's transl)].

Observations obtained by psychopathologic examination and some psychologic testing of two patients in the course of amnesic episodes (transient global amnesia) are presented and discussed. In both cases the psychopathologic findings are those of a reversible isolated amnesic syndrome, characterized by diffuse retrograde amnesia and recent memory deficit, whereas immediate and remote (personal) memory are preserved. Stereotype questions, disorientation in time, and--in one case--anxious restlessness, which accompany the amnesic syndrome, are probably due to impaired memory and the patient's awareness of it. This typical syndrome allows differentiation of amnesic episodes from other types of amnesia. In the first case, which had been under clinical observation from the beginning to the end of the amnesic episode, a special evolution of the event could be ascertained. The acute amnesic episode reached its climax with a certain delay and thereafter decreased gradually. It can be presumed that--at least during the remission phase in the second case--the ability of recall is impaired rather than that of registration and retention. Other findings obtained in the second case--and compared with observations in the literature--point out that in the phase of remission the timespan of retrieval seems to become longer and, in respect to previously applied sensory modalities, improves in a different manner.

Aged↗
PubMed1976

Pentylenetetrazol-induced amnesia: a case for overt seizures.

In this study, the possible role of overt convulsions following pentylenetetrazol (PTZ) in retrograde amnesia was investigated. Following a single passive avoidance conditioning, when overt convulsions were blocked with sodium pentobarbital (Nem), the amnesic effect of pentylenetetrazol was also blocked. Subconvulsive doses of the drug did not produce amnesia. Animals that received a typically convulsive dose of the drug but failed to convulse were not amnesic; only animals with overt convulsions were different from saline controls. The data suggest that overt convulsions may be necessary for the development of pentylenetetrazol-induced retrograde amnesia.

Amnesia↗
PubMed1984

Electroconvulsive shock and brain muscarinic receptors: relationship to anterograde amnesia.

Rats were administered one electroconvulsive shock daily for 7 days (ECS X 7) and were killed 24 hours after the last treatment. Muscarinic cholinergic receptor number, as determined by [3H] quinuclidinyl benzilate [( 3H]QNB) binding, was significantly reduced in the cerebral cortex. A parallel group of rats was trained on a passive avoidance task 24 hours following the last ECS and tested for retention of the original avoidance response 24 hours later; these animals exhibited a profound amnesia. Animals tested 1 hour following training were not amnestic, indicating that learning was unimpaired. Animals trained 7 days following ECS X 7 were not amnestic and [3H] QNB binding changes were not demonstrable at this time. A single ECS which does not significantly affect cortical [3H] QNB binding, did not induce amnesia in rats trained 24 hours after the treatment and tested 24 hours later. The parallel, cumulative nature of ECS-induced muscarinic receptor down-regulation and ECS-induced anterograde amnesia suggests a possible causative relationship.

Amnesia↗
PubMed1984

The effects of sulfated and nonsulfated cholecystokinin octapeptides on electroconvulsive shock-induced retrograde amnesia after intracerebroventricular administration in rats.

The effects of several doses of intracerebroventricularly injected cholecystokinin octapeptide sulfate ester (CCK-8-SE) and nonsulfated scholecystokinin octapeptide (CCK-8-NS) were studied on electroconvulsive shock (ECS)-induced retrograde amnesia, as measured in a one-trial step-through passive avoidance paradigm. Both CCK-8-SE and CCK-8-NS were able to attenuate amnesia slightly when they were injected into rats 10 min prior to ECS treatment, possibly by reducing the severity of the ECS-induced seizures. Of the treatments carried out immediately after ECS, only the 0.8 pmole dose of CCK-8-NS could significantly restore retrograde amnesia. After treatment 20 min prior to testing 24-hr retention, no effect of the peptides was observed. The lack of a dose-dependency and of any effect on retrieval raises the possibility that the CCK octapeptides influence memory processes by an indirect mechanism.

Amnesia↗
PubMed1988

Priming of semantic autobiographical knowledge: a case study of retrograde amnesia.

The case of a 36-year-old man who suffers dense retrograde and anterograde amnesia as a result of closed-head injury that caused extensive damage to his left frontal-parietal and right parieto-occipital lobes is described. Patient K.C. has normal intelligence and relatively well-preserved perceptual, linguistic, short-term memory, and reasoning abilities. He possesses some fragmentary general knowledge about his autobiographical past, but he does not remember a single personal event or happening from any time of his life. He has some preserved expert knowledge related to the work he did for 3 years before the onset of amnesia, although he has no personal recollections from that period. Some features of K.C.'s retrograde amnesia can be interpreted in terms of the distinction between episodic and semantic memory, and in terms of the distinction between episodic and semantic autobiographical knowledge. K.C.'s semantic knowledge, but not his episodic knowledge, showed progressive improvement, or priming, in the course of the investigation.

Adult↗
PubMed2006

Anterograde and retrograde amnesia in a person with bilateral fornix lesions following removal of a colloid cyst.

AD, a 45-year-old man, presented with a severe and global anterograde amnesia following surgery for removal of a colloid cyst. Structural neuroimaging confirmed bilateral lesions to the fornix and a small lesion in the basal forebrain. Testing for remote episodic memory of autobiographical events, and for remote semantic memory of personal and public events, and of famous people, revealed that AD had a severe retrograde amnesia for autobiographical episodes that covered his entire lifetime, and a time-limited retrograde amnesia for semantic memory. Because the fornix and basal forebrain lesions disrupted major afferent and efferent pathways of the hippocampus, it was concluded that the integrity of the hippocampus and its projections are needed to retain and/or recover autobiographical memories no matter how old they are. By contrast, hippocampal contribution to semantic memory is time-limited. These findings were interpreted as consistent with Multiple Trace Theory, which holds that the hippocampal system is essential for recovering contextually rich memories no matter how old they are, but is not needed for recovering semantic memories.

Amnesia, Anterograde↗
PubMed1982

Retrograde amnesia for forty years.

We describe a patient who, in the absence of anterograde amnesia, experienced sudden onset of profound retrograde amnesia for the last forty years of his life. The amnesia encompassed all knowledge, including motor skills, acquired during these forty years. There has been no recovery in over eighteen months. His symptoms seem most consistent with a vascular etiology. Current understanding of memory disorders fails to explain these symptoms. It may be that his case represents a previously undescribed disorder.

Activities of Daily Living↗
PubMed1987

Length of retrograde amnesia after head injury: a revised formula.

Our earlier retrospective study presented a formula relating lengths of retrograde amnesia to length of post-traumatic amnesia (PTA) and length of time since injury (Crovitz, Horn and Daniel, 1983). The earlier study derived the formula from 27 cases with retrograde amnesia. The present study adds another 75 cases, and we discuss similarities and differences between the two samples.

Adult↗
PubMed1976

Retrograde amnesia in honeybees (Apis mellifera carnica).

After a single reward on a spectral color, freely flying honeybees show retrograde amnesia when an electroconvulsive shock, CO2 narcosis, N2 narcosis, or cooling (to 1 degrees C) is applied after learning. Retrograde amnesia is measurable with these four treatments up to 7 min after the reward. For none of the treatments was a consistent relationship found between the reaction tested and the time of testing after the treatment. Prolonged application of the four treatments leads to a significant increase in the rate of retrograde amnesia only after CO2 narcosis. Memory in the honeybee is susceptible to impairment until 15 min after the reward.

Amnesia↗
PubMed2001

Hippocampal amnesia.

This article reviews 147 cases of amnesia following damage including the hippocampus or fornix as reported in 179 publications. The aetiology, mnestic abilities and reference(s) are tabulated for each case. Consistent findings across cases include the association of bilateral hippocampal damage with a deficit in anterograde episodic memory combined with spared procedural and working memory. The limited nature of retrograde amnesia following lesions to the fornix is also noted. Less consistent and thus more controversial findings, include effects of lesion size or laterality, deficits in semantic memory or familiarity-based recognition and the extent of retrograde amnesia. The evidence concerning these issues is reviewed across cases.

Amnesia↗
PubMed2001

Generalized dissociative amnesia: episodic, semantic and procedural memories lost and found.

OBJECTIVE: This review tests Ribot's classic twofold categorization of generalized amnesia (GA) into Type I, total loss of episodic memory, and Type II, additional more or less extensive loss of semantic and/or procedural memory. It also explores his law of regression, according to which, cast in modern terms, recovery of lost procedural and semantic memories precedes recovery of episodic memory, as well as reported aetiological factors. METHOD: Clinically and formally assessed cases of GA, published since 1845, were surveyed and further analysed. RESULTS: Over and above authentic episodic memory loss, cases differed widely in the extent of impairment of semantic and procedural memory. Recovery of semantic and procedural memory often preceded recovery of episodic memory. This particularly applied to authenticated trauma memories. To an extent, lost memories affected current functioning, and in some cases were associated with alternating dissociative personalities. Severe memory distortions upon memory recovery were not reported. Most cases were trauma or stress related, while in some cases the aetiology remained unknown. CONCLUSIONS: Contrary to the view expressed in DSM-IV, which states that dissociative amnesia pertains to an inability to recall personal information, GA may also involve loss and recovery of semantic and procedural memories. Since the loss of various memory types in GA is dimensional rather than categorical, Ribot's typological distinction does not hold. Some of the reviewed cases suggest a trauma-related aetiology. Generalized amnesia of varying degrees of severity can involve delayed retrieval of trauma memories, as well as the loss and delayed retrieval of the premorbid personality.

Amnesia↗
PubMed2002

Isoflurane causes anterograde but not retrograde amnesia for pavlovian fear conditioning.

BACKGROUND: Production of retrograde amnesia by anesthetics would indicate that these drugs can disrupt mechanisms that stabilize memory. Such disruption would allow suppression of memory of previous untoward events. The authors examined whether isoflurane provides retrograde amnesia for classic (Pavlovian) fear conditioning. METHODS: Rats were trained to fear tone by applying three (three-trial) or one (one-trial) tone-shock pairs while breathing various constant concentrations of isoflurane. Immediately after training, isoflurane administration was either discontinued, maintained unchanged, or rapidly increased to 1.0 minimum alveolar concentration for 1 h longer. Groups of rats were similarly trained to fear context while breathing isoflurane by applying shocks (without tones) in a distinctive environment. The next day, memory for the conditioned stimuli was determined by presenting the tone or context (without shock) and measuring the proportion of time each rat froze (appeared immobile). For each conditioning procedure, the effects of the three posttraining isoflurane treatments were compared. RESULTS: Rapid increases in posttraining isoflurane administration did not suppress conditioned fear for any of the training procedures. In contrast, isoflurane administration during conditioning dose-dependently suppressed conditioning (P < 0.05). Training to tone was more resistant to the effects of isoflurane than training to context (P < 0.05), and the three-trial learning procedure was more was more resistant than the one-trial procedure (P < 0.05). CONCLUSIONS: Isoflurane provided intense dose-dependent anterograde but not retrograde amnesia for classic fear conditioning. Isoflurane appears to disrupt memory processes that occur at or within a few minutes of the conditioning procedure.

Acoustic Stimulation↗
PubMed2004

A primate model of anterograde and retrograde amnesia produced by convulsive treatment.

A nonhuman primate model of the key cognitive effects of convulsive treatment was developed and tested. Rhesus macaques were trained on 3 tasks: a long-term memory task that required selection of a constant target from a background of distracters, an anterograde task that involved learning a new target each day against a variable number of distracters, and a task that assessed learning and memory for new and previously trained 3-item serial lists. This battery samples a range of cognitive functions, including orientation, working memory, retrograde amnesia for temporally graded stimuli, and anterograde amnesia. Using a within-subject, sham-controlled design, the amnestic effects of electroconvulsive shock (ECS) were evaluated in 2 monkeys. Significant effects of the interventions (sham and ECS) were seen on all tasks. The degree of impairment varied across tasks and as a function of task difficulty. ECS did not impair accuracy on the less difficult tasks (memory for an overlearned item and acquisition of a new item) but did increase the amount of time required to complete the tasks, consistent with a period of disorientation acutely after the intervention. This effect was progressive across the treatments. ECS impaired the acquisition and memory of new lists compatible with an anterograde memory deficit, whereas recall for old lists was relatively spared. This study developed and validated a cognitive battery to assess amnesia in nonhuman primates, providing new experimental paradigms for evaluating the cognitive effects of convulsive treatment.

Amnesia, Anterograde↗
PubMed1964

ELECTROCONVULSIVE SHOCK, RETROACTIVE AMNESIA, AND THE SINGLE-SHOCK METHOD.

If electroconvulsive shock is given immediately after a learning session, retroactive amnesia for that response occurs. Such results may be due to production of aversive responses or to interference with consolidation of the neural engram, or to both. Aversive responses or competing responses are not adequate explanations for retroactive amnesia. Consolidation theory provides the most plausible explanation. The single-shock method is an appropriate approach for studying the relationships between electroconvulsive shock and retroactive amnesia.

Amnesia↗
PubMed1978

Retrograde amnesia produced by several treatments: evidence for a common neurobiological mechanism.

This experiment examined the effects on memory of various amnestic treatments in animals earlier treated with the alpha-adrenergic antagonist phenoxybenzamine (PBZ). Thirty minutes before being trained in a one-trial inhibitory (passive) avoidance task, animals received an injection of PBZ or saline. Immediately after training, each animal received one of the following amnestic treatments: stimulation of the frontal cortex or amygdala, pentylenetetrazol, diethyldithiocarbamate, or cycloheximide. In control animals, each treatment produced retrograde amnesia. However, PBZ-treated animals did not develop amnesia. These findings suggest that there may be a common neurobiological mechanism underlying the amnesias produced by many treatments.

Amnesia↗