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PubMed2004

Malingering and retrograde amnesia: the historic case of the Collegno amnesic.

Assessment of feigned cognitive disorders is an important field of neuropsychology because of its applications to forensic settings. Strategies for detecting malingering in amnesia are available for anterograde amnesia. Less attention has been given to malingering in retrograde amnesia. The case of the 'Smemorato di Collegno' (The Collegno Amnesic) is probably the most famous case of malingered retrograde amnesia ever known in Italy. In 1926, a man who appeared to have lost all his autobiographical memories and identity spent nearly a year in the Collegno asylum of Turin without a name. He was later initially identified as Giulio Canella, Director of the 'Scuola Normale di Verona' who had disappeared during the war in 1916. He was suspected of later identified as being Mario Bruneri, a petty crook from Turin who played the part of an amnesic whose retrograde memory gradually returned. A lengthy investigation was required before this conclusion was reached. Several clinicians and renowned academics evaluated the case, but only Alfredo Coppola, diagnosed "malingered retrograde amnesia" using a method that was extremely innovative for the times. The aim of the present paper is to review the original cognitive evaluation and the strategies used for malingering detection in the "Collegno case". The outcome of the case is then discussed in the light of present-day forensic neuropsychology and the level of advancement of mental examination achieved in the 1920s in Europe is highlighted.

Amnesia, Retrograde↗
PubMed2005

Retrograde amnesia: neither partial nor complete hippocampal lesions in rats result in preferential sparing of remote spatial memory, even after reminding.

Many lesion experiments have provided evidence that the hippocampus plays a time-limited role in memory, consistent with the operation of a systems-level memory consolidation process during which lasting neocortical memory traces become established [see Squire, L. R., Clark, R. E., & Knowlton, B. J. (2001). Retrograde amnesia. Hippocampus 11, 50]. However, large lesions of the hippocampus at different time intervals after acquisition of a watermaze spatial reference memory task have consistently resulted in temporally ungraded retrograde amnesia [Bolhuis, J. J., Stewart, C. A., Forrest, E. M. (1994). Retrograde amnesia and memory reactivation in rats with ibotenate lesions to the hippocampus or subiculum. Quarterly Journal of Experimental Psychology 47B, 129; Mumby, D. G., Astur, R. S., Weisend, M. P., Sutherland, R. J. (1999). Retrograde amnesia and selective damage to the hippocampal formation: memory for places and object discriminations. Behavioural Brain Research 106, 97; Sutherland, R. J., Weisend, M. P., Mumby, D., Astur, R. S., Hanlon, F. M., et al. (2001). Retrograde amnesia after hippocampal damage: recent vs. remote memories in two tasks. Hippocampus 11, 27]. It is possible that spatial memories acquired during such a task remain permanently dependent on the hippocampus, that chance performance may reflect a failure to access memory traces that are initially unexpressed but still present, or that graded retrograde amnesia for spatial information might only be observed following partial hippocampal lesions. This study examined the retrograde memory impairments of rats that received either partial or complete lesions of the hippocampus either 1-2 days, or 6 weeks after training in a watermaze reference memory task. Memory retention was assessed using a novel 'reminding' procedure consisting of a series of rewarded probe trials, allowing the measurement of both free recall and memory reactivation. Rats with complete hippocampal lesions exhibited stable, temporally ungraded retrograde amnesia, and could not be reminded of the correct location. Partially lesioned rats could be reminded of a recently learned platform location, but no recovery of remote memory was observed. These results offer no support for hippocampus-dependent consolidation of allocentric spatial information, and suggest that the hippocampus can play a long-lasting role in spatial memory. The nature of this role--in the storage, retrieval, or expression of memory--is discussed.

Amnesia, Retrograde↗
PubMed2004

On Common Ground: Jost's (1897) law of forgetting and Ribot's (1881) law of retrograde amnesia.

T. Ribot's (1881) law of retrograde amnesia states that brain damage impairs recently formed memories to a greater extent than older memories, which is generally taken to imply that memories need time to consolidate. A. Jost's (1897) law of forgetting states that if 2 memories are of the same strength but different ages, the older will decay more slowly than the younger. The main theoretical implication of this venerable law has never been worked out, but it may be the same as that implied by Ribot's law. A consolidation interpretation of Jost's law implies an interference theory of forgetting that is altogether different from the cue-overload view that has dominated thinking in the field of psychology for decades.

Amnesia, Retrograde↗
PubMed1982

Aging-related changes in retrograde amnesia for mice.

Aging mice showed a retrograde amnesia for passive avoidance behavior when a single electroconvulsive shock (ECS) was given at post-training intervals up to 1 h, whereas adult mice showed no significant amnesia when ECS was given 10 min or more after training. Catecholamines (norepinephrine and dopamine), but not serotonin (5-HT) changed with aging in the several brain regions, but only 5-HT was significantly changed (elevated) by ECS. Protein synthesis was significantly inhibited by ECS, notably in limbic structures. The increased susceptibility of aging mice to the amnesic effect of ECS could be related to aging-related changes in the rate of memory consolidation or to the duration of neural chemical changes that disrupt processes such as consolidation, storage, and/or retrieval of the memory trace.

Aging↗
PubMed2001

Long-term retrograde amnesia...the crucial role of the hippocampus.

For patients with hippocampal pathology, disagreement exists in the literature over whether retrograde amnesia is temporally limited or very extensive depending on whether the anatomical damage is restricted to this structure or also involves additional temporal cortex. We report a comprehensive assessment of retrograde and anterograde memory functions of a severely global amnesic patient (VC). We found that he presented with a remarkably extensive and basically ungraded retrograde amnesia. This impairment profoundly affected four decades preceding the onset of his amnesia and encompassed both non personal and personal facts and events. VC also presented with a severe anterograde amnesia and a deficit in the acquisition of new semantic knowledge in the post-morbid period. Detailed MRI volumetric measurements revealed gross abnormalities in both hippocampi which were markedly shrunken. Of relevance to the debate on retrograde amnesia were the observations that the volumes of both entorhinal cortices and the remainder of both temporal lobes were normal. These data suggest that the hippocampus is critical not only for the efficient encoding and hence normal recall of new information but also for the recall of episodic information acquired before the onset of amnesia. Our results are compatible with the view that retrograde amnesia is both extensive and ungraded when the damage is limited to the hippocampus.

Aged↗
PubMed2005

Retrograde amnesia for semantic information in Alzheimer's disease.

Patients with mild to moderate Alzheimer's disease and normal controls were tested on a retrograde amnesia test with semantic content (Neologism and Vocabulary Test, or NVT), consisting of neologisms to be defined. Patients showed a decrement as compared to normal controls, pointing to retrograde amnesia within semantic memory. No evidence for a gradient within this amnesia was found, although one was present on an autobiographic test of retrograde amnesia that had a wider time scale. Several explanations for these results are presented, including one that suggests that extended retrograde amnesia and semantic memory deficits are in fact one and the same deficit.

Aged↗
PubMed1987

Differential susceptibility to anterograde and retrograde amnesia treatments in preweanling rats.

Although there have been several reports that preweanling rats and mice are relatively resistant to experimentally induced retrograde amnesia, there is virtually no information concerning susceptibility to anterograde amnesia in subjects of this age. Therefore, in the present experiment, 23-day-old rats received hypothermia either prior to, or immediately after, punishment training in an attempt to induce anterograde and retrograde amnesia, respectively. When tested 24 hr later, only those subjects given hypothermia prior to training exhibited any loss of retention. Thus these results confirmed previous evidence of resistance to retrograde amnesia in preweanling rats and further demonstrated that substantial anterograde amnesia could be obtained in these subjects. Performance of subjects tested after a 5-min retention interval revealed that the poor retention performance in subjects cooled prior to training and tested 24 hr later was not due to a learning deficit. These results are also discussed with respect to the issue of the independence of anterograde and retrograde amnesia.

Amnesia↗
PubMed2003

Perirhinal cortex lesions produce variable patterns of retrograde amnesia in rats.

Two experiments examined the contribution of the perirhinal cortex (PRh) to retrograde memory for the location of a platform in a water maze. In a previous study, we found that electrolytic lesions of the PRh produced retrograde amnesia, without a temporal gradient, for water-maze problems acquired 4 weeks and 2 days before surgery [Behav. Brain. Res. 114 (2000) 119]. In Experiment 1, we used the same mixed design as in our previous report (time of learning was a within-subjects factor), but PRh lesions were made by aspiration. Contrary to our earlier report, these PRh rats displayed good retention of both platform locations. Combined, these findings indicate that the lesion method may contribute importantly to the pattern of deficits observed. Experiment 2 was conducted similar to Experiment 1, except that a completely between-subjects design was used (time of learning was a between-subjects factor). Rats that received PRh lesions approximately 2 days after the last training session displayed impaired retention of the platform's location, whereas rats that received PRh lesions 4 weeks after training did not. This finding of a temporally graded retrograde amnesia is consistent with our earlier report, and further suggests that the involvement of the PRh in the retention of water-maze problems is time-limited. However, also consistent with our earlier report, the PRh-lesioned rats in Experiment 2 that displayed a retention deficit rapidly reacquired the task. This finding, combined with the negative findings in Experiment 1, suggests that the contribution of the PRh to retrograde memory for platform locations is subtle and may not be due to impaired spatial memory abilities. Additionally, the conflicting results of Experiments 1 and 2 underscore the importance of the design employed in studies of retrograde amnesia in animals.

Amnesia, Retrograde↗
PubMed1994

Post-traumatic retrograde amnesia with selective impairment of autobiographical memory.

A selective, temporally limited retrograde amnesia, confined to autobiographical memory, was the only sequela of a "minor" head trauma in two young men. The retrograde memory gap covered about one year of life before the trauma and persisted for several months, without any anterograde deficit or other cognitive disturbances. This unusual pattern of retrograde amnesia deserves close consideration and points to the dissociation of memory subsystems and mechanisms.

Adult↗
PubMed1999

Retrograde amnesia: clinical and methodological caveats.

Several clinical and methodological caveats are outlined as they pertain to retrograde amnesia research, and data relevant to these caveats are presented. Three caveats in particular are noted in relation to recently published cases of marked retrograde amnesia; (i) temporal lobe epilepsy may influence memory for news events; (ii) there may be additional, unsuspected pathology in cases of amnesia, such as those with cerebral hypoxia; (iii) degree of media exposure is closely related to performance on the types of news events memory tests that are commonly used in retrograde amnesia research.

Adult↗
PubMed1995

A new case of retrograde amnesia with abnormal forgetting rate.

The classic amnesic syndrome is characterised by a severe anterograde amnesia and a less important retrograde amnesia with sparing of the semantic component. We report the case of a patient who showed a global amnesic syndrome following a mild head injury. Initially, amnesia was both anterograde and retrograde, and also involved semantic knowledge. Two years later the picture had changed remarkably. The retrograde deficit for autobiographical events was still total, while semantic memory had recovered to a large extent. Learning had also greatly improved, but only if assessed after a short delay; abnormally rapid forgetting rate were found at longer intervals. This pattern of impairment does not lend itself to an easy interpretation. However, the hypothesis of a consolidation deficit may be advanced.

Adolescent↗
PubMed2006

Glucocorticoid mechanisms may contribute to ECT-induced retrograde amnesia.

RATIONALE: Cortisol levels rise sharply immediately after electroconvulsive therapy (ECT); the resultant stimulation of steroid receptors in the hippocampus may be beneficial or harmful to cognition, depending on the magnitude of the stimulation. Steroid mechanisms may therefore modulate ECT-induced amnesia. OBJECTIVES: Using mifepristone (a glucocorticoid receptor antagonist) as a chemical probe, we sought to examine steroid mechanisms in an animal model of ECT-induced retrograde amnesia. MATERIALS AND METHODS: Adult, male Wistar rats (n = 68) trained in a step-through passive-avoidance task were randomized to receive mifepristone (20 or 40 mg kg(-1) day(-1)) or vehicle (control). These treatments were administered 1 day before the electroconvulsive shock (ECS) course and, again, 1 h before each of five once-daily true (30 mC) or sham ECS. Recall of pre-ECS learning was tested 1 day after the last ECS. RESULTS: Relative to sham ECS, true ECS resulted in significant retrograde amnesia in the vehicle group but not in either of the mifepristone groups. In sham ECS-treated animals, mifepristone did not significantly influence recall. In ECS-treated rats, the higher but not the lower dose of mifepristone was associated with significant protection against the retrograde amnesia evident in the vehicle group. CONCLUSION: Mifepristone administered before the ECT seizure may attenuate ECT-induced retrograde amnesia. This suggests that glucocorticoid mechanisms may contribute to ECT-induced retrograde amnesia.

Amnesia, Retrograde↗
PubMed1999

Temporally-specific retrograde amnesia in two cases of discrete bilateral hippocampal pathology.

The role of the hippocampus in retrograde amnesia remains controversial and poorly understood. Two cases are reported of discrete bilateral hippocampal damage, one of which was a rare case of limbic encephalitis secondary to the human herpes virus 6. Detailed memory testing showed marked anterograde memory impairment, but only mild, temporally-limited retrograde amnesia that covered a period of several years in both autobiographical and factual knowledge domains. The absence of extensive retrograde amnesia in these two cases points to a time-limited role for the hippocampus in the retrieval of retrograde memories, and suggests that entorhinal, perirhinal, parahippocampal, or neocortical areas of the temporal lobe may be more critical than the hippocampus proper for long-term retrograde memory functioning. Our findings offer general support to theories of memory consolidation that propose a gradual transfer of memory from hippocampal to neocortical dependency.

Adult↗
PubMed1992

Actors but not scripts: the dissociation of people and events in retrograde amnesia.

We describe our further investigations of the retrograde amnesia in a single case. R.F.R. became globally amnesic following an attack of Herpes Simplex Encephalitis. He could generate and recognize superordinate level information about the vast majority of proper names including the names of people but he was very impaired at giving information about what had "happened" to these same individuals. He could also provide detailed information about family friends but he could not recall salient major personal episodes in which these same individuals had been involved. Knowledge of people appears to be represented in a different way to that of events, even when a singular event has provided the main or only opportunity for learning about the individual.

Amnesia, Retrograde↗
PubMed1985

Disrupting circadian rhythms in rats induces retrograde amnesia.

Disrupting circadian organization in rats by phase-shifting the illumination cycle or by exposure to a reversed day/night cycle or to continuous light, resulted in retrograde amnesia for passive avoidance behavior. This retrograde amnesia induced by phase-shifting lasted at least 2 days, and gradually diminished the longer the rats were exposed to the new illumination cycle. Retention performance was not impaired when rats were exposed to phase-shifting for 3-5 days before the learning trial. The retrograde amnesia due to changing the illumination cycle is probably due to retrieval disturbances. Extinction of active avoidance behavior was facilitated in rats exposed to a phase-shifted illumination cycle, but social and explorative behavior of rats tested in dyadic encounters were not affected by changing the normal illumination cycle. It is concluded that phase-shifting may result in amnesia for newly learned behavioral responses, but not for more innate behavioral patterns.

Amnesia↗
PubMed1995

Isolated retrograde amnesia for autobiographical material associated with acute left temporal lobe encephalitis.

Retrograde amnesia for autobiographical material in the absence of anterograde amnesia or other memory disturbances was found in a patient with acute viral encephalitis. Memory loss showed a temporal gradient, but new learning was spared. Both brain perfusion imaging with 99mTc-HMPAO SPECT, and EEG localized the lesion in the left temporal lobe while CT and MRI were normal. This observation supports the anatomical differentiation between the different memory functions. The uncommon combination of isolated retrograde amnesia without other neuropsychological findings may raise the doubt of psychogenic aetiology, which in this case was refuted.

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↗