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PubMed1980

Selecting retrieval cues for early-childhood amnesia: implications for the study of shrinking retrograde amnesia.

A method for selecting semantic cues for early childhood memories is presented. The written records of episodes submitted by the subjects in the study of Crovitz and Harvey (1979) were coded into three-word strings of words in accordance with the gist of the memories. Nouns which described many retrievals (Set A) and nouns which had described few retrievals (Set B) were presented to an independent group of young adults as prompts for early childhood episodes. Prompting with semantic cues gave a fast rate of retrieval, with nouns in Set A cuing early childhood memories more successfully than nouns in Set B. The difference between words in Set A and Set B was found not to be a function of the frequency of usage of these words in the language. Implications for selecting cues to prompt retrieval of memories during the period of shrinking retrograde amnesia are discussed.

Adult↗
PubMed1983

[Effect of mental stimulants on electroconvulsive shock-induced retrograde amnesia].

The effect of nootropics on the retrograde amnesia induced by electroshock was studied on a model of the active conditioned escape reaction (pole jumping). In untreated animals the daily application of electroshock for three days, immediately after the training, led to a significant retardation of the development of a conditioned escape reaction. The administration of nootropics influences the development of the retrograde amnesia to different extents, the treatment regimen (application of the drug only during the training and supplementary pretreatment before the first day of training; respectively) being of importance. The antiamnestic effect of Piracetam (100 mg/kg, intraperitoneally) which is good also without pretreatment, may still be potentiated, especially on the fourth day of treatment, by an additional administration of the drug, beginning four days before the first day of treatment. In contrast to this, meclofenoxate hydrochloride (100 mg/kg, intraperitoneally) and pyritinol (100 mg/kg, intraperitoneally) produce a marked inhibition of the development of the retrograde amnesia only after pretreatment. Without pretreatment these drugs exert a slight or no effect. The marked antiamnestic effect of methylglucaminorotate (225 mg/kg, intraperitoneally) and by an additional pretreatment. As to dihydroergotoxin (1 mg/kg; intraperitoneally), both treatment regimens were ineffective in the model used.

Amnesia, Retrograde↗
PubMed1984

Retrograde amnesia in Parkinson's disease.

Retrograde amnesia was assessed in demented and non-demented Parkinson's patients using a test of remote memory spanning the years from 1920-1979. Results indicated that the demented patients 1) scored significantly below normal controls and 2) had equal impairment for all time periods. This pattern was like that seen in other dementing illnesses (i.e., Huntington's and Alzheimer's diseases), but different from that in amnesic disorders, such as Korsakoff's syndrome. The data, therefore, suggest qualitative differences in pattern of remote memory loss between the dementias and amnesic syndromes.

Aged↗
PubMed1979

Early childhood amnesia: a quantitative study with implications for the study of retrograde amnesia after brain injury.

Measurement of retrieval of episodic memories ascribed to the various years of early childhood was made over a three-month period of search by 17 normal young adults. The distribution of episodes ascribed to various ages is described, and it is shown that the recovery of memory from early childhood tends to show features of shrinking retrograde amnesia. Methods which were used to recover very early episodes are described, and implications for the study of shrinking retrograde amnesia in brain-damaged patients are discussed.

Adult↗
PubMed1996

A case of simulated, psychogenic or focal pure retrograde amnesia: did an entire life become unconscious?

A case of pure retrograde amnesia following mild head injury is reported. Neuropsychological, psychodynamic and statistical approaches are employed in an attempt to disentangle the clinical picture presented by the patient. Focal retrograde amnesia, psychogenic retrograde amnesia and simulated amnesia are all taken into account. From a public events questionnaire and an inquiry about famous people, consistency analyses showed that the patient was able implicitly to use information she denied having, but at the same time, made us lower the probability of a simulated amnesia. Moreover, psychodynamic analysis showed that the patient's personality structure was compatible with hysterical patterns and we suggest that the patient's memory defect may be related to her personality. It seems less likely, though still possible, that the case may be explained in terms of deliberate simulation. In this case we conclude that the classification along the conscious/unconscious dimension seems more informative than the contrast between psychogenic and organic genesis.

Adult↗
PubMed1992

The dissociation of anterograde and retrograde amnesia in a patient with herpes encephalitis.

Establishing the precise relationship between anterograde amnesia (AA) and retrograde amnesia (RA) has implications for psychological and neuroanatomical models of memory. Many patients have been described who demonstrate AA in conjunction with RA or who demonstrate AA with little, or no apparent, RA. Intact anterograde memory in conjunction with deficits on tasks of retrograde memory is rarely encountered. In this paper, we describe a young female patient (LD) whose RA is extremely severe when contrasted with her mild to moderate deficits on tasks of verbal anterograde memory. In addition, on tests of episodic and semantic autobiographical memory, LD appeared more impaired in her recall of specific episodes than of factual information about her past. The importance of this dissociation in RA for the episodic-semantic distinction and the possible role of visual imagery in recalling remote episodic events are discussed.

Adult↗
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↗
PubMed1999

Syndromes of retrograde amnesia: a conceptual and empirical synthesis.

This article attempts a synthesis of the range of disorders that have been subsumed under the rubric of retrograde amnesia. At a functional level, it is possible to make distinctions between various forms of retrograde amnesia, including a distinction between episodic amnesia for personally experienced events and semantic retrograde amnesia for components of knowledge, such as those relating to people and events. At an anatomical level, discrete lesions to limbic-diencephalic structures usually result in a limited degree of retrograde amnesia. Marked episodic or marked semantic retrograde amnesia is usually associated with significant involvement of cortical and neocortical structures. Retrograde amnesia is a functionally heterogeneous rather than a unitary phenomenon. Discontinuities and dissociations found in published studies point to the potential fractionation of retrograde amnesia into component disorders, each with its own neural profile.

Amnesia, Retrograde↗
PubMed2001

Isolated and focal retrograde amnesia: a hiatus in the past.

Two cases of isolated retrograde amnesia were reported. Both showed the same clinical pattern in development and resolution of amnesia despite of different etiologies. Sudden insult to the brain (trauma in Case 1 and viral encephalitis in Case 2) caused concurrent antero- and retrograde amnesia. Fortunately both recovered from the anterograde amnesia completely. However, both were left with a period of postictal amnesia of a few months and retrograde amnesia of up to 14 months' duration. The analysis of their pattern of temporal evolution and dissolution of amnesia support the hypothesis that recently acquired episodic information requires a certain amount of constant activation for a certain period of time in order to be organized into a durable memory. The nature of this activation as well as its origin remains to be solved.

Accidents, Traffic↗
PubMed1999

Ketaset-Rompun extends the temporal gradient for hypothermia-induced retrograde amnesia.

In studies of experimentally induced retrograde amnesia (RA), as the interval between training and the amnestic treatment is lengthened, amnesia decreases (4). This temporal gradient for RA has been reported with a wide variety of amnestic agents, including RA produced by thermoregulatory disturbances (8). This temporal gradient for RA is not unlike certain characteristics of classical conditioning, where weaker conditioned responding occurs when the interval between the conditioned stimulus (CS) and unconditioned stimulus (US) is lengthened. Furthermore, there is evidence that administration of anesthetics can lengthen the "effective conditioning" interval between the CS and US, as demonstrated in a conditioned taste-aversion (CTA) procedure (10). In that study, little conditioning was observed when a 3-h delay (or more) was incorporated between presentations of the CS (flavor) and the US (toxin). However, if subjects were anesthetized immediately after the CS was delivered and remained anesthetized during the CS-US interval, strong conditioning was observed with CS-US intervals of up to 9 h. The aim of the present experiment was to determine if the temporal gradient for hypothermia-induced RA could also be lengthened. That is, we tested whether the interval between training and hypothermia treatment could be lengthened by anesthetizing subjects with Ketaset-Rompun. The results indicate that the training-to-amnestic agent interval could be lengthened within moderate limits. The implications for hypothermia-induced RA is further discussed.

Adrenergic alpha-Agonists↗
PubMed1996

A study of recovery of memory function in a case of witnessed functional retrograde amnesia.

We describe a case of transient functional retrograde amnesia that had features of a fugue state, and that was accompanied by loss of personal identity and significant autobiographical amnesia. Uniquely, we were able to gather information from witnesses who observed the episode from its onset, and we were also able to monitor the acute stages of recovery of memory function over the subsequent four-week period. The profile of memory loss was characterised by impaired performance on both autobiographical and public events memory tasks, in the context of normal anterograde memory test scores. Shrinkage of retrograde amnesia took place over a four-week period, with autobiographical and public events components of retrograde memory recovering at the same rate. We discuss the possible role of unconscious processes underlying the episode, as compared to conscious simulation. We argue that most cases of functional retrograde amnesia may represent a combination of conscious simulation and unconscious processes.

Journal Article↗
PubMed2006

[Comparison of retrograde amnesia changes within different injury levels of cerebral concussion in rats].

OBJECTIVE: To investigate the retrograde amnesia changes within different injury levels of cerebral concussion in rats. METHODS: A metallic pendulum striker device of brain injury was deployed to duplicate CC models of different injury levels within Sprague-Dawley (S-D) rats. The investigated animals were divided into two groups according to classification standard, that is, Pure Cerebral Concussion (PCC) group and Complicated Cerebral Concussion (CCC) group. One control group was used, and each group included 8 animals. The retrograde amnesia of each group was assessed by Morris Water Maze (MWM) Test from 3 days preinjury to 7 days postconcussion. RESULTS: Compared with the control group, the retrograde amnesia was detected within 3 days in PCC group, and 5 days in CCC group after injury. At the same time, the two groups both manifested space recognition deficit. CONCLUSION: The retrograde amnesia existed in both pure cerebral concussion group and complicated cerebral concussion. Furthermore, the lasting time of retrograde amnesia in animals correlates to the injury level of brain concussion.

Amnesia, Retrograde↗
PubMed2001

H.M., word knowledge, and aging: support for a new theory of long-term retrograde amnesia.

This study develops a new theory of long-term retrograde amnesia that encompasses episodic and semantic memory, including word knowledge. Under the theory, retrograde amnesia in both normal individuals and hippocampal amnesics reflects transmission deficits caused by aging, nonrecent use of connections, and infrequent use of connections over the life span. However, transmission deficits cause severe and irreversible retrograde amnesia only in amnesics who (unlike normal persons) cannot readily form new connections to replace nonfunctioning ones. The results of this study are consistent with this theory: For low-frequency but not high-frequency words, a famous "hippocampal amnesic" (H.M.) at age 71 performed worse than memory-normal control participants in a lexical decision experiment and a meaning-definition task (e.g., What does squander mean?). Also as predicted, H.M.'s lexical decision performance declined dramatically between ages 57 and 71 for low-frequency words, but was age-invariant for high-frequency words.

Age Factors↗
PubMed1974

Recovery from retrograde amnesia: a learning process.

Retrograde amnesia was produced in rats by electroconvulsive shock. Memory recovered if the animals were given repeated test trials. Memory did not recover if steps were taken to reduce the conditioning properties of the test trials; the manipulations included eliminating the response, altering the apparatus cues, or extinguishing conditioned "fear" by confining animals to the apparatus during the first test trial.

Amnesia↗
PubMed1992

Isolated prolonged retrograde amnesia.

We describe a patient who had isolated retrograde amnesia of 1-year duration without anterograde amnesia after recovery from encephalitis. Single photon emission computed tomography using 123I-IMP revealed that left temporal lobe abnormality. We postulate that the learning ability for new information and recalling ability for old information involve different neural structures, and there is a possible relationship between isolated retrograde amnesia and left temporal dysfunction.

Adult↗
PubMed1999

Disproportionate retrograde amnesia in a patient with herpes simplex encephalitis.

We describe a patient who developed a severe but temporally limited retrograde amnesia coupled with a relatively mild anterograde amnesia following herpes simplex encephalitis. The patient showed a profound retrograde amnesia for autobiographical events extending for about 10 years prior to the disease onset. Her knowledge about public events and famous persons was also impaired for this period. An MRI and SPECT demonstrated bilateral medial temporal pathology. This case represents a further instance of a relatively focal retrograde amnesia following brain damage. We review other reported cases with focal retrograde amnesia and consider theoretical and neuroanatomical accounts for the present case. Two factors may account for her amnesic patterns: a partial disruption of the store for premorbid binding codes (i.e., information that multimodal feature representations occurred synchronously); along with a relative preservation of the encoding process required to develop new synchronous codes.

Acyclovir↗