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At least 19 recordsLinked to original sources

PubMed1997

Transient global amnesia and functional retrograde amnesia: contrasting examples of episodic memory loss.

We studied 11 patients with transient global amnesia (TGA) and ten patients with functional retrograde amnesia (FRA). Patients with TGA had a uniform clinical picture: a severe, relatively isolated amnesic syndrome that started suddenly, persisted for 4-12 h, and then gradually improved to essentially normal over the next 12-24 h. During the episode, the patients had severe anterograde amnesia for verbal and non-verbal material and retrograde amnesia that typically covered at least two decades. Thirty hours to 42 days after the episode, the patients had recovered completely and performed normally on tests of anterograde and retrograde amnesia. By contrast, patients with FRA had a sudden onset of memory problems that were characterized by severe retrograde amnesia without associated anterograde amnesia and with a clinical presentation that otherwise varied considerably. The episodes persisted from several weeks to more than two years, and some of the patients had not recovered at the time of our last contact with them. The uniform clinical picture of TGA and the variable clinical picture of FRA presumably reflect their respective neurologic ('organic') and psychogenic ('non-organic') aetiologies.

Amnesia↗

PubMed1998

Episodic memory and the self in a case of isolated retrograde amnesia.

Isolated retrograde amnesia is defined as impaired recollection of experiences pre-dating brain injury with relatively preserved anterograde learning and memory. We present findings from a patient (M.L.) with isolated retrograde amnesia following severe traumatic brain injury (TBI) that address hypotheses of the interrelationships of focal neuropathology, episodic memory and the self. M.L. is densely amnesic for experiences predating his injury, but shows normal anterograde memory performance on a variety of standard tests of recall and recognition. The cognitive processes underlying this performance were examined with the remember/know technique, which permits separation of episodic from non-episodic contributions to memory tests by quantifying subjects' reports of re-experiencing aspects of the encoding episode. The results demonstrated that M.L. does not episodically re-experience post-injury events to the same extent as control subjects, although he can use familiarity or other non-episodic processes to distinguish events he has experienced from those he has not experienced. M.L.'s MRI showed damage to the right ventral frontal cortex and underlying white matter, including the uncinate fasciculus, a frontotemporal band of fibres previously hypothesized to mediate retrieval of specific events from one's personal past. Recent functional neuroimaging evidence of an association between right frontal lobe functioning and episodic retrieval demands suggest that M.L.'s memory deficits are related to this focal injury. This hypothesis was supported by right frontal polar hypoactivation in M.L. in response to episodic retrieval demands when he was examined with a cognitive activation H2(15)O PET paradigm that reliably activated this frontal region in both healthy controls and patients with TBI carefully matched to M.L. (but without isolated retrograde amnesia). He also showed increased left inferomedial temporal activation relative to control subjects, suggesting that his spared anterograde memory is mediated through increased reliance on medial temporal lobe structures. Re-experiencing events as part of one's past is based on autonoetic awareness, i.e. awareness of oneself as a continuous entity across time. This form of awareness also supports the formulation of future goals and the implementation of a behavioural guidance system to achieve them. The findings from this study converge to suggest that M.L. has impaired autonoetic awareness attributable to right ventral frontal lobe injury, including right frontal-temporal disconnection. Reorganized brain systems mediate certain preserved cognitive operations in M.L., but without the normal complement of information concerning the self with respect to both past and future events.

Adult↗

PubMed2002

Anterograde amnesia and temporally graded retrograde amnesia for a nonspatial memory task after lesions of hippocampus and subiculum.

We studied the importance of the hippocampus and subiculum for anterograde and retrograde memory in the rat using social transmission of food preference, a nonspatial memory task. Experiment 1 asked how long an acquired food preference could be remembered. In experiment 2, we determined the anterograde amnesic effects of large lesions of the hippocampus that included the subiculum. In experiment 3, large lesions of the hippocampus that included the subiculum were made 1, 10, or 30 d after learning to determine the nature and extent of retrograde amnesia. Normal rats exhibited memory of the acquired food preference for at least 3 months after learning. Hippocampal lesions that included the subiculum produced marked anterograde amnesia and a 1-30 d temporally graded retrograde amnesia. The results show the importance of the hippocampus and related structures for nonspatial memory and also demonstrate the temporary role of these structures in long-term memory.

Amnesia, Anterograde↗

PubMed2001

Right medial thalamic lesion causes isolated retrograde amnesia.

Pervasive retrograde amnesia without anterograde memory impairment has rarely been described as a consequence of circumscribed brain damage. We report this phenomenon in a 33 yr-old, right-handed man (JG) in association with the extension in the right thalamus of a previously small, bilateral thalamic lesion. JG presented with a dense amnesia for autobiographical material more than a few years old, with some sparing of recent memories. Furthermore, he was completely unable to recognise famous people or world events. Many other aspects of semantic knowledge were intact and there was no evidence of general intellectual impairment, executive dysfunction or loss of visual imagery. Magnetic resonance imaging revealed an acute lesion in the right thalamus and two small, symmetrical, bilateral non-acute thalamic lesions. Follow-up neuropsychological assessment indicated a stable pattern of impaired retrograde and spared anterograde memory over 18 months and psychiatric assessments yielded no evidence of confabulation, malingering or other symptoms to suggest psychogenic amnesia. JG's profile indicates that the division of declarative memory into just two categories - episodic and semantic - is inadequate. Rather, his case adds to the growing body evidence to suggest that world knowledge pertaining to people and events is stored or accessed similarly to autobiographical information and differently from other types of more general factual knowledge. We hypothesize that the right mediodorsal thalamic nucleus and immediately surrounding regions comprise the central processing mechanism referred to by McClelland (Revue Neurologique, 150 (1994) 570) and Markowitsch (Brain Research Review, 21 (1995) 117) as responsible for inducing and co-ordinating the recall of these sorts of cortically stored memory engrams.

Adult↗

PubMed1989

[A case of retrograde amnesia of 22 years, continued for 4 days following a general anesthesia accompanied by a permanent amnesia of these 4 days after the complete recovery from the retrograde amnesia].

A case of global amnesia which continued for 4 days following a general anesthesia and recovered without any neurological deficits was reported. The patient was a 38-year-old woman suspected of lung cancer, and scheduled for pulmonary lobectomy. She had a history of appendectomy under spinal anesthesia 22 years before. She was premedicated with diazepam (10mg), atropine (0.5mg) and pentazocine (30mg). Anesthesia was induced with thiamylal (500mg) and succinylcholine (140mg) iv and 100% oxygen. Anesthesia was maintained with enflurane and nitrous oxide with oxygen for 3 hours. After her recovery from anesthesia, a retrograde amnesia of 22 years was observed and continued for 4 days. Then the memory was restored completely, but the amnesia during these 4 postoperative days remained permanently. We have documented the case of amnesia in the immediate postoperative period which is similar to transient global amnesia. It seems likely that this amnesia was caused by drug interaction, hypoxia, decreased cerebral perfusion or psychogenic effects of general anesthesia.

Adult↗

PubMed2002

Focal retrograde amnesia documented with matching anterograde and retrograde procedures.

Focal retrograde amnesia is an unusual and theoretically challenging form of memory disorder. The case of a 65-year-old woman presenting with focal retrograde amnesia is reported. Following a cardiac arrest and subsequent hypoxia she remained in a coma for 24 h with evidence of epileptiform activity during the early recovery period. MR scans, 4 and 7 months post-onset, showed mild bifrontal atrophic changes mainly affecting white matter areas. An [18F]fluorodeoxyglucose resting PET scan 1-year post-onset demonstrated right occipito-temporo-parietal hypometabolism. We were able to document the patient's performance on an extensive range of anterograde and retrograde tests and to monitor her recovery of function by assessing her performance at 4, 12 and 24 months post-onset. Spared anterograde memory was observed on a range of verbal and non-verbal tests, including matched tasks that compared pre-illness and post-illness onset recollections. In contrast, her performance on retrograde memory tests, using detailed autobiographical and public events verbal and photographic tasks, showed a temporally-graded retrograde amnesia, more particularly affecting memory for autobiographical episodes. Possible mechanisms underlying CH's focal retrograde amnesia are discussed in terms of Damasio's time-locked multiregional retroactivation model.

Aged↗

PubMed2001

The loss of episodic memories in retrograde amnesia: single-case and group studies.

Retrograde amnesia in neurological disorders is a perplexing and fascinating research topic. The severity of retrograde amnesia is not well correlated with that of anterograde amnesia, and there can be disproportionate impairments of either. Within retrograde amnesia, there are various dissociations which have been claimed-for example, between the more autobiographical (episodic) and more semantic components of memory. However, the associations of different types of retrograde amnesia are also important, and clarification of these issues is confounded by the fact that retrograde amnesia seems to be particularly vulnerable to psychogenic factors. Large frontal and temporal lobe lesions have been postulated as critical in producing retrograde amnesia. Theories of retrograde amnesia have encompassed storage versus access disruption, physiological processes of 'consolidation', the progressive transformation of episodic memories into a more 'semantic' form, and multiple-trace theory. Single-case investigations, group studies and various forms of neuroimaging can all contribute to the resolution of these controversies.

Amnesia, Retrograde↗

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↗

PubMed1988

Transient global amnesia: characterization of anterograde and retrograde amnesia.

Five patients with transient global amnesia (TGA) were given neuropsychological tests during and after their episode. During TGA, all patients were impaired on tests of new learning ability for both verbal and nonverbal material. Retrograde amnesia was patchy and covered a variable period of time before the onset of the episode: from about 36 hours in one case to 4 years in two cases. Some cognitive impairment in addition to amnesia was present during the episode. For example, patients copied a complex figure more poorly during the episode than afterwards. All patients had normal memory at follow-up testing. These data are consistent with the idea that the amnesic symptoms of TGA are caused by transient bilateral dysfunction of medial temporal brain structures important for memory.

Aged↗

PubMed1989

Transient global amnesia: evidence for extensive, temporally graded retrograde amnesia.

We gave six patients with transient global amnesia (TGA) neuropsychological tests during and after their episodes. During TGA, all patients had severe anterograde amnesia for verbal and nonverbal material and a patchy but temporally graded retrograde amnesia for personal and public events dating back to at least 1960. In addition, they were unusually passive during TGA, had impaired ability to copy a complex figure, and possibly had mild impairment of confrontation naming. All exhibited complete recovery of memory and other cognitive abilities after the episode. There are similarities between the transient amnesia of patients with TGA and the chronic amnesia of patients with presumed bilateral damage to the medial temporal region or the diencephalic midline.

Amnesia↗

PubMed2003

Role of platelet activating factor in triazolobenzodiazepines-induced retrograde amnesia.

Benzodiazepine (diazepam), triazolobenzodiazepines (brotizolam, triazolam) and platelet activating factor (PAF) antagonist (BN 52021) are administered to mice before acquisition and retrieval trials conducted using Morris water maze. Benzodiazepine has produced only anterograde amnesia and it has not produced retrograde amnesia. Triazolobenzodiazepines have produced both anterograde and retrograde amnesia. PAF antagonist (BN 52021) has only produced retrograde amnesia and it has not produced anterograde amnesia. The anterograde amnesia produced by benzodiazepine and triazolobenzodiazepines, has been prevented by benzodiazepine receptor antagonist (flumazenil). It suggests that benzodiazepine- and triazolobenzodiazepines-induced anterograde amnesia may be mediated through benzodiazepine receptors. On the other hand, retrograde amnesia produced by PAF antagonist (BN 52021) and triazolobenzodiazepines has been attenuated by PAF and PAF acetyl hydrolase inhibitors such as cigarette smoke extract (CSE) and phenylmethanesulfonylflouride. It suggests that triazolobenzodiazepine-induced retrograde amnesia may be mediated through blockade of PAF receptors.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗

PubMed2001

Retrograde amnesia.

In humans, the phenomenon of temporally graded retrograde amnesia has been described in the clinic and the laboratory for more than 100 years. In the 1990s, retrograde amnesia began to be studied prospectively in experimental animals. We identified 13 published studies in which animals were given equivalent training at two or more separate times before damage to the fornix or hippocampal formation. Eleven of these studies found temporally graded retrograde amnesia, with the extent of amnesia ranging from several days to a month or two. We consider these studies and also suggest why temporally graded retrograde amnesia has sometimes not been observed. Although the evidence in favor of temporally graded retrograde amnesia is substantial, the inference from this work, that memory is reorganized as time passes, is rather vague and depends on mechanisms yet to be identified. It is therefore encouraging that many opportunities exist for moving beyond purely descriptive studies to studies that involve treatments or manipulations directed toward yielding information about mechanisms.

Amnesia, Retrograde↗

PubMed1986

Amnesia can facilitate memory performance: evidence from a patient with dissociated retrograde amnesia.

A case is reported of a patient who experienced numerous episodes of transient global amnesia (TGA) during which anterograde amnesia was less prominent than usual, and who developed a permanent selective retrograde amnesia. On formal testing, he performed well on traditional verbal memory tests, but showed marked retrograde amnesia for verbal material, including items on a famous voices recognition test. He was administered a paired-associate learning test where the names of famous personalities for which he was amnesic were associated with incongruous activities (e.g. John Newcombe-singing). Our patient performed better on this task than a group of five matched control subjects. Our observations indicate that in the organization of human memory retrograde amnesia may be fractionated from anterograde amnesia and that in certain situations specific types of amnesia can produce a facilitation effect compared to the performance of control subjects.

Aged↗

PubMed1995

Retrograde amnesia and memory consolidation: a neurobiological perspective.

The fact that information acquired before the onset of amnesia can be lost (retrograde amnesia) has fascinated psychologists, biologists, and clinicians for over 100 years. Studies of retrograde amnesia have led to the concept of memory consolidation, whereby medial temporal lobe structures direct the gradual establishment of memory representations in neocortex. Recent theoretical accounts have inspired a simple neural network model that produces behavior consistent with experimental data and makes these ideas about memory consolidation more concrete. Recent physiological and anatomical findings provide important information about how memory consolidation might actually occur.

Amnesia, Retrograde↗

PubMed1999

Postencephalitic focal retrograde amnesia after bilateral anterior temporal lobe damage.

BACKGROUND: Marked retrograde amnesia with no or almost no anterograde amnesia is rare. Recently, a combination of ventrolateral prefrontal and temporopolar cortical lesions has been suggested as the cause of such isolated or focal retrograde amnesia. It is also assumed that when the right-sided cortical structures are damaged, autobiographical episodic memories are affected. OBJECTIVE: To search for new anatomic substrates for focal retrograde amnesia. METHODS: We performed extensive neuropsychological tests and obtained detailed neuroimages on a 43-year-old woman who showed a severe, persistent retrograde amnesia but only a limited anterograde amnesia after probable herpes simplex encephalitis. RESULTS: Tests of autobiographical memory revealed that she had a memory loss extending back to her childhood for both semantics and incidents; however, the ability to recall specific episodes appeared much more severely impaired than the ability to recall factual information about her past. The patient also showed profound impairments in recalling public memories; however, her scores improved nearly to a control level on forced-choice recognition memory tasks, although the recall of memories for a decade just before her illness remained mildly impaired. MRI revealed focal pathologies in the temporal poles and the anterior parts of the inferotemporal lobes on both sides, predominantly on the left, with some extension to the anterior parts of the medial temporal lobes. There was additional damage to the left insular cortex and its surrounding structures but no evidence of frontal lobe damage on MRIs or cognitive tests. CONCLUSIONS: A profound retrograde amnesia may be produced by damage to the bilateral temporal poles and anterior inferotemporal lobes in the absence of frontal lobe pathologies, and a dense and persistent episodic old memory loss can arise even with a relatively small lesion in the right anterior temporal lobe if it is combined with extensive damage to the left.

Adult↗

PubMed1984

[Post-traumatic retrograde amnesia].

A case of post traumatic retrograde amnesia is described. The patient presented after an initial coma a global amnesia, but the fixation deficit rapidly disappeared, and a severe retrograde amnesia dating back to childhood experience and learning remained the main symptom. Amnesia for remote events was associated with didactic memory deficit and, at a lesser degree, with a verbal memory deficit. Recovery of fixation allowed a progressive relearning. This pattern of impairment was recently related to mesencephalic lesions, but we think that the role of temporal lobe involvement cannot be neglected.

Adult↗

PubMed1989

The neurology of memory: quantitative assessment of retrograde amnesia in two groups of amnesic patients.

The phenomenon of retrograde amnesia has important implications for understanding normal memory as well as its neural organization. Using 6 tests of remote memory, we evaluated the extent and severity of retrograde amnesia in 2 groups of amnesic patients--7 patients with alcoholic Korsakoff's syndrome and 5 other patients with amnesia (anoxia or ischemia, N = 3; thalamic infarction, N = 1; unknown etiology, N = 1). Although there were individual differences, Experiment 1 showed that the severity and extent of retrograde amnesia was similar for the 2 groups. Retrograde amnesia was temporally graded across a period of about 15 years and was not detectable in more remote time periods. In Experiment 2, repeated testing during a 3 year period showed that amnesic patients and control subjects were similarly consistent in their responses. Amnesic patients did not catch up to control subjects by eventually accumulating as many correct answers as the control subjects. In Experiment 3, amnesic patients performed normally on a test of very difficult general information questions, which were based on material likely to have been learned long ago. In all 3 experiments, the 2 groups of amnesic patients performed similarly. The results support the following conclusions: (1) Extensive, temporally graded retrograde amnesia, which has been observed frequently in patients with Korsakoff's syndrome, occurs readily in other amnesic patients as well, even when their memory impairment appears well circumscribed; (2) patients with presumed damage to either the medial temporal or the diencephalic brain structures linked to memory functions can produce a similar kind of retrograde amnesia; (3) the impairment reflects a loss of usable knowledge, not simply difficulty accessing an intact memory store that can then be overcome given sufficient retrieval opportunities; (4) very remote memory, at least for factual information, can be intact in amnesia; (5) the structures damaged in amnesia support memory storage, retrieval, or both during a lengthy period of reorganization, after which representations in memory can become independent of these structures.

Alcohol Amnestic Disorder↗

PubMed1993

Focal retrograde amnesia in neurological disease: a critical review.

The condition of focal retrograde amnesia represents a new and challenging concept to our understanding of human memory disorders. Cases of both permanent and transient focal retrograde amnesia, dating from early clinical descriptions to more recent experimental reports, are critically reviewed. It is concluded that the condition of focal retrograde amnesia does represent a distinct and reliable neurological entity. Four sets of issues are discussed--methodological issues, conceptual issues, anatomical issues and therapeutic issues. Current evidence indicates an important role for temporal lobe structures in mediating focal retrograde amnesia. Both storage and retrieval deficits may contribute to the presence of focal retrograde amnesia, though available evidence points to a greater role for engram destruction/fragmentation rather than disruption of access mechanisms. In general, pharmacological and other therapies have had minimal effects in alleviating focal retrograde amnesia.

Amnesia↗