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PubMed2006

Is dissociative amnesia a culture-bound syndrome? Findings from a survey of historical literature.

BACKGROUND: Natural human psychological phenomena, such as depression, anxiety, delusions, hallucinations and dementia, are documented across the ages in both fictional and non-fictional works. We asked whether 'dissociative amnesia' was similarly documented throughout history. METHOD: We advertised in three languages on more than 30 Internet web sites and discussion groups, and also in print, offering US$1000 to the first individual who could find a case of dissociative amnesia for a traumatic event in any fictional or non-fictional work before 1800. RESULTS: Our search generated more than 100 replies; it produced numerous examples of ordinary forgetfulness, infantile amnesia and biological amnesia throughout works in English, other European languages, Latin, Greek, Arabic, Sanskrit and Chinese before 1800, but no descriptions of individuals showing dissociative amnesia for a traumatic event. CONCLUSIONS: If dissociative amnesia for traumatic events were a natural psychological phenomenon, an innate capacity of the brain, then throughout the millennia before 1800, individuals would presumably have witnessed such cases and portrayed them in non-fictional works or in fictional characters. The absence of cases before 1800 cannot reasonably be explained by arguing that our ancestors understood or described psychological phenomena so differently as to make them unrecognizable to modern readers because spontaneous complete amnesia for a major traumatic event, in an otherwise lucid individual, is so graphic that it would be recognizable even through a dense veil of cultural interpretation. Therefore, it appears that dissociative amnesia is not a natural neuropsychological phenomenon, but instead a culture-bound syndrome, dating from the nineteenth century.

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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↗
PubMed1987

Transient global amnesia. When memory temporarily disappears.

Transient global amnesia is a benign condition of sudden onset that resolves spontaneously. Retrograde amnesia prevents recall of events antedating the episode by hours to years, and anterograde amnesia produces the characteristic features of inability to learn new material and repetitious questioning. Laboratory investigation of these patients is generally unrewarding. Transient global amnesia is easily distinguished from amnesia caused by head trauma or transient ischemic attack, confusional state, and functional amnesia. Although transient global amnesia is most likely caused by transient ischemia of brain structures important for memory, thromboembolic cerebrovascular disease is not the cause. The patient with transient global amnesia should be treated conservatively.

Amnesia↗
PubMedDate not supplied

An individual patient comparison of response to a memory training program--psychogenic V organic amnesia: brief report.

Psychogenic amnesia ("dissociative amnesia" in DSM-IV) has received relatively little attention in the literature. We compared neuropsychological and behavioral findings between a patient with psychogenic amnesia and one with organic amnesia from their early stages in a rehabilitation program. A 52-yr-old man developed anterograde and retrograde amnesia and short-term memory disturbance 1 mo after an operation for esophageal carcinoma, with no loss of personal identity and information. No apparent organic causes were identified, but because the patient and his wife rejected psychiatric treatment and memory deficit characteristics were compatible with that of an organic origin, the patient was referred to a physiatrist. A 46-yr-old man with anterograde amnesia was diagnosed with limbic encephalitis based on findings of magnetic resonance imaging and single-photon emission computed tomography, which showed lesions in both medial temporal lobes. Both patients underwent "memory book" training because they showed preserved performance in motor learning tasks. The first patient's responses to training contrasted with the other's and were indicative of psychogenic amnesia, with cancer representing a precipitating stress. Counseled by the physiatrist, the patient and his wife accepted suggestions to undergo psychiatric treatment. We propose that it is important to consider behavioral responses to memory rehabilitation as well as neuropsychological findings in differentiating psychogenic amnesia from an organic one and that physiatrists may be pivotal in diagnosing and initiating treatment in such psychiatric disorders.

Amnesia↗
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↗
PubMed1997

Measurement of post-traumatic amnesia: how reliable is it?

OBJECTIVE: To develop and test a clinical protocol for determining post-traumatic amnesia by retrospective questioning. To establish its limits and factors which influence reliability. DESIGN: Two independent assessments using the Rivermead post-traumatic amnesia protocol were undertaken by separate observers on various groups of patients at various time intervals. Analysis investigated the correlations between assessments, the percentage difference between assessments, the number of patients changing category, and the differences between these analyses in the different patient subgroups. Assessments were undertaken both in hospital and in the patients' homes. Four different patient groups were studied. These were group A: 12 inpatients with very severe head injury late after injury; Group B: 40 patients interviewed at home six months after injury; group C: 22 patients interviewed within a few weeks of injury at home; group D: 116 patients interviewed initially within a few weeks and then at six months, on both occasions at home. The Rivermead post-traumatic amnesia protocol involved clinical questioning of the patient to establish how long after injury (in hours/days/weeks) the patient regained continuous day to day memory. All periods of coma were included. Severity was categorised with standard criteria. RESULTS: Overall correlation was good (Spearman's r 0.79), but the correlation was lower for patients with post-traumatic amnesia < 24 hours and when there was a long delay between assessments. In all groups 19%-25% of patients changed categories between assessments, but only 2% changed by two categories. CONCLUSIONS: The assessment of post-traumatic amnesia with the Rivermead post-traumatic amnesia protocol is reasonably reliable. The misclassification rate however, is significant enough that some caution should be taken in individual cases. Other evidence does show post-traumatic amnesia to be valid, and it probably remains the best simple prognostic item available. In clinical practice one should avoid placing too much weight on post-traumatic amnesia alone.

Adult↗
PubMed1997

Diencephalic temporal order amnesia.

OBJECTIVE: Amnesia for temporal relations may occur without amnesia for content memories. The aim was to determine whether a patient with mild memory loss due to a thalamic lesion had amnesia for temporal relations, and whether the amnesia was specific for particular material. METHODS: A male patient had an isolated right dorsomedial thalamic infarct and resolving amnesia. He was tested on tasks relating to content (what) and temporal (when) memories for both verbal and non-verbal material, three and seven months after his infarct. RESULTS: Three months after his infarct, the man had amnesia for temporal, but not content memories using non-verbal stimuli, and normal performance using verbal stimuli. Seven months after his infarct, he had a normal performance using verbal and non-verbal stimuli. CONCLUSIONS: Patients with thalamic lesions may have a material specific amnesia for temporal relations in the absence of amnesia for content.

Adult↗
PubMed1998

Transient amnesia after perimesencephalic haemorrhage: the role of enlarged temporal horns.

OBJECTIVES: Although long term outcome of patients with perimesencephalic haemorrhage, a benign subset of subarachnoid haemorrhage, is excellent, some patients report an episode of amnesia for the first hours to days after the ictus. The relation between the occurrence of amnesia and the size of the ventricles on CT, including the temporal horns, were studied in patients with perimesencephalic haemorrhage. METHODS: Twenty seven consecutive patients with perimesencephalic haemorrhage were asked about the occurrence of amnesia. Age adjusted bicaudate indices and third ventricle sizes were calculated. Linear measurements of the temporal horn were taken in three directions: anterior-posterior, medial-lateral, and oblique. Additionally, enlargement of the temporal horns was assessed with the "naked eye". RESULTS: Ten of the 27 patients reported an episode of transient amnesia; in these patients the mean sizes of the temporal horns were larger than in patients without amnesia, ranging from a factor of 1.7 for the medial-lateral measurement to a factor of 2.3 for the anterior-posterior measurement. Most of the patients with amnesia had relative bicaudate indices and relative third ventricle sizes> 1, and all had enlarged temporal horns at "naked eye" assessment. CONCLUSION: About one third of patients with perimesencephalic haemorrhage have an episode of amnesia shortly after the bleed. The occurrence of amnesia is associated with enlargement of the temporal horns, and might be explained by temporary hippocampal dysfunction.

Aged↗
PubMed2000

[Transient global amnesia].

UNLABELLED: A DISTINCTIVE SYNDROME: Transient global amnesia is a very distinctive amnesic syndrome. The attack begins abruptly with massive anterograde verbal and non-verbal amnesia. Retrograde amnesia, variable in extent, is also present. A repetitive questioning behavior is usual. The memory impairment gradually resolves after almost always less than 12 hours. WELL-DEFINED CRITERIA: Specific criteria make it possible to distinguish transient global amnesia from psychogenic amnesia, acute confusional state and transient epileptic amnesia. "Pure" transient global amnesia is usually idiopathic and has a good prognosis. It is also distinguishable from symptomatic transient global amnesia. PATHOGENESIS: Functional imaging studies detect hippocampic or thalamic hypoperfusion. This oligemia may be secondary to neuronal dysfunction compatible with spreading depression. The pathogenic mechanisms remain unclear.

Amnesia, Transient Global↗
PubMedDate not supplied

Midazolam sedation for upper gastrointestinal endoscopy: comparison between the states of patients in partial and complete amnesia.

BACKGROUND/AIMS: The amnesia produced by anesthesia is advantageous for unpleasant procedures like gastroscopy, and midazolam is one of the most commonly used anesthesias for endoscopy. However the proper use of midazolam from the viewpoint of complete amnesia has been discussed very little. METHODOLOGY: One hundred and thirty-three unselected patients about to undergo upper gastrointestinal endoscopy were premedicated with sufficient intravenous midazolam to cause enough sedation so that no response was evoked when calling their name. Pulse, arterial pressure, arterial oxygen saturation and the physical signs of patients were recorded continuously during the procedures. After the study, patients were given 0.25 mg of flumazenil and asked if they could recall the procedures. Those who could recall even part of the procedure were not regarded as achieving complete amnesia. The efficacy of the sedative was judged by the appearance of complete amnesia. RESULTS: From our regression analysis complete amnesia was achieved in 75.9% of the total patients. The differences of the blood pressure fall, pulse rate increase and arterial oxygen saturation fall between the patients with complete and partial amnesia were minute and did not cause serious complications. Regression analysis revealed the most important factors for the complete amnesia to be midazolam dose per body weight and habitual hypnotic use. CONCLUSIONS: There are no obvious disadvantages to producing complete amnesia with midazolam for upper gastrointestinal endoscopy. Habitual hypnotic use along with midazolam dose per body weight is the most influencing factor for that purpose.

Amnesia↗
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↗
PubMed1975

The von Restorff effect and induced amnesia: production by manipulation of sound intensity.

When an outstanding item appears in an otherwise homogeneous list of items, the outstanding item is better remembered (the von Restorff effect), and items before and after it may be more poorly remembered (induced amnesia) than corresponding items in a control list. In the present experiments the outstanding item was a word presented as a loud shout among other words presented at normal conversational levels. In two experiments, large retrograde- and anterograde-induced amnesiae effects were demonstrated using a free-recall and a recognition task. In both experiments half of the subjects were told what to expect and were instructed to devise a strategy to eliminate induced amnesia. These instructions failed to eliminate the amnesiac effect. A third experiment was designed to demonstrate an empirical similarity between induced and clinical amnesia. In clinical retrograde (but not anterograde) amnesia, "lost" memories are sometimes recovered with time. Filled delays of 0, 30, or 120 sec interpolated between list presentation and recall demonstrated that induced retrograde amnesia disappeared at the longest delay but induced anterograde amnesia was unchanged. A fourth experiment eliminated some alternate interpretations of the effect.

Adult↗
PubMed1996

Amnesia in acute herpetic and nonherpetic encephalitis.

OBJECTIVES: To evaluate how often global amnesia syndrome is encountered as a sequel of herpes simplex virus type 1 encephalitis (HSVE) and in other types of acute encephalitides, and to evaluate whether there are qualitative differences in amnesia caused by different encephalitides. SUBJECTS: Forty-five consecutive patients with encephalitis (mean age, 40.8 years) studied prospectively within a 5-year period, 8 of whom had HSVE. There were 24 normal controls. MEASURES: Neuropsychological assessment and memory evaluation after the acute stage of encephalitis, as well as at follow-up after 27.7 +/- 18.6 months. RESULTS: Three patients (6%), including 1 with HSVE, had persistent anterc grade and retrograde memory defects, typical features of global amnesia. Twelve patients had anterograde amnesia in the first assessment. No statistically significant differences in the memory measures were found between the HSVE (n = 4) and the non-HSVE (n = 8) groups. Some patients had predominantly semantic difficulty, some had a "frontal-type" memory disorder, and in some patients rapid forgetting was the prominent feature. CONCLUSIONS: The frequency of amnesia can reliably be evaluated only in consecutive series of patients. Previous literature, mainly case reports, may give the impression that global amnesia is a common consequence of encephalitis. Our findings do not support that view. Furthermore, there are clear differences in the quality of the memory impairment between cases of acute encephalitides. Our findings suggest that amnesia as a consequence of encephalitis, even HSVE, should not be considered a uniform phenomenon.

Acute Disease↗
PubMed1988

Animal model studies of benzodiazepine-induced amnesia.

The development of a mouse passive avoidance test as a model for amnesia produced by benzodiazepines is described. The model appropriately classifies the amnesic potential of a wide range of psychoactive drugs as validated by clinical findings. Control experiments indicate that the effect is best described as anterograde amnesia resulting from a failure of consolidation. gamma-Aminobutyric acid (GABA) antagonists had almost no effect on benzodiazepine-induced amnesia, whereas the benzodiazepine-receptor antagonist Ro 15-1788 completely and specifically reversed it. This clinically confirmed finding suggests that benzodiazepine-induced amnesia is mediated through the benzodiazepine-receptor. However, in vivo inhibition of benzodiazepine binding does not correlate well with amnesia in the mouse, and some benzodiazepine-receptor agonists with potent CNS effects in other in vitro models do not produce amnesia. Additional work is needed to clarify what aspects of benzodiazepine receptor occupancy mediate amnesia.

Amnesia↗
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↗
PubMed1998

Focal retrograde amnesia associated with vascular headache.

We report the case of a 42-year-old man with repeated attacks of headache associated with retrograde amnesia. Neuropsychological tests before and after the major episode of amnesia showed mild neuropsychological deficits but with spared anterograde memory and learning functions. The amnesia was dense for a period of 15-20 years and included people and events (public and private). There was also a suggestion of amnesia for learned skills. Neurologically he had mild clinical signs and focal EEG-abnormalities in the left fronto-temporal region, but CT, MRI, and SPECT showed no abnormality. Five years after the onset of amnesia there was no recovery of the retrograde memory deficit, but a PET (glucose) scan was normal and neuropsychological testing showed no deficits. An association with migraine has been reported for some non-classical amnesias, but this is the first case of selective retrograde amnesia in a patient with headache as a primary neurological diagnosis.

Amnesia, Retrograde↗
PubMed1983

Attenuation of cycloheximide-induced amnesia in mice with strychnine sulfate.

Two experiments were conducted to determine the effectiveness of strychnine sulfate in attenuating the amnesia induced in mice by small doses of cycloheximide (CYC). Previously, reversal of CYC-induced amnesia catecholamine agonists has been taken as evidence that protein synthesis inhibitors induce amnesia via an inhibition of catecholamine synthesis. The results of Experiment 1 suggested that strychnine sulfate could attenuate an amnesia induced by 30 mg/kg CYC, and the results of Experiment 2 revealed that even the robust amnesia induced by 75 mg/kg CYC could be attenuated by strychnine sulfate. The results of these experiments support the results of previous experiments which showed that agents having little or no effect on the catecholamines can nonetheless attenuate amnesia induced by the protein synthesis inhibitors. Thus, some method other than attenuation of the retention deficit by catecholamine agonists must be used to test the hypothesis that protein synthesis inhibitors induce amnesia via an inhibition of catecholamine synthesis.

Amnesia↗
PubMed2006

Basal forebrain amnesia: a case study.

OBJECTIVE: To provide new evidence of the existence of basal forebrain amnesia, as a different entity from hippocampal or diencephalic amnesia. BACKGROUND: Some authors consider that the characteristics of amnesia do not depend on lesion site, although others claim there are neuropsychologic differences between amnesias due to hippocampal, diencephalic, and basal forebrain lesions. As to the latter, literature is scarce and controversial. The opportunity to thoroughly study J.S., a man with a high IQ and amnesia, enabled us to reinforce the second hypothesis. METHODS: J.S. is a 47-year-old man who underwent surgery for a pituitary adenoma, the resulting lesion involving only the basal forebrain. We gave him a complete neuropsychologic battery for amnesia and executive functions. RESULTS: J.S. showed severe amnesia with a flat learning curve, a rapid forgetting rate and good recognition, a temporal gradient of several years for remote memory, preserved semantic and procedural memory. Most of the tests for executive functions were normal, although he did have a significant personality change after surgery. CONCLUSIONS: This patient is different from patients with hippocampal or diencephalic lesions, and is similar to other patients reported with basal forebrain lesions. The main difference is the relation between his flat learning curve and preserved recognition, both for visual and verbal material.

Adenoma↗