[On the importance of initial amnesia in the evaluation of injury consequences. (Cerebral traumatic amnesia)].
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Adolescent↗
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[Amnesia. Transient global amnesia].
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Aged↗
Pituitary hormones and amnesia.
Pituitary hormones profoundly influence behavior through direct actions on the brain. One of these behavioral effects is the attenuation of experimental amnesia. Traditionally, amnesia is considered as a "loss of memory." Memory comprises at least 2 stages: input (memory consolidation) and output (memory retrieval). Theoretically, disturbance of either aspect of memory may be the cause of amnesia. Also, it is possible that amnesia is based on a factor or factors not related to memory. Data and theories on amnesia in man were reviewed. Some salient features were mentioned: (1) amnesia can be induced by a variety of agents; (2) amnesia covers periods ranging from seconds to years; (3) amnesia gradients can be established; (4) amnesia is to a large extent reversible. From this survey, it seems possible that amnesia is not a homogeneous phenomenon and that even in one person a disturbance of both memory consolidation and memory retrieval may be produced by one and the same event. Animal studies in general have confirmed these conclusions. We have developed an animal model in order to study the effects of pituitary peptides on amnesia. This model is based on CO2-induced amnesia for a one-trial passive avoidance response in rats. This amnesia could be attenuated by treatment with ACTH-analogs 1 hour before the retrieval test. This anti-amnesic effect of ACTH-analogs was not dependent on the nature of the behavioral response or the amnesic treatment. The vasopressin-analog DGLVP similarly exerted an anti-amnesic effect when injected before the retrieval trial. In contrast to ACTH-analogs, however, it also reduced the amnesia when injected before acquisition. These results suggest that amnesia may comprise a "faulty-consolidation" and a "faulty-retrieval" component, which may be amended by different pituitary hormones. The study of the anti-amnesic activity of peptides therefore not only serves to characterize the nature of the behavioral effect of these peptides but may also prove to be helpful of the unraveling of processes involved in amnesia.
Adrenocorticotropic Hormone↗
[A clinical study of generalized amnesia].
Six cases of generalized amnesia were reported. Generalized amnesia caused by phenomena of genuinely psychogenic origin is a rare psychological disorder and spontaneous recovery from amnesia in a comparatively short period of time is one of the characteristics of this disorder. Three of the cases in this report developed amnesia which was prolonged in comparison with previously reported cases. A comparison between these six cases and previously reported cases of amnesia elucidated the general characteristics of this disorder, differential diagnosis from other disorders, the development of a new identity during the amnestic period, amnesia as an alternative to suicide, factors related to prolonged amnesia, and its treatment. Although differential diagnosis from other disorders, especially from malingering, is sometimes difficult, the patient's attitude toward amnesia, the development of the clinical course of amnesia, the premorbid personal history, and interpersonal relationships should be carefully observed and evaluated in order to differentiate generalized amnesia from malingering. During the amnestic period it was observed that three of the cases believed that they had names of other persons, and two of them recalled personal histories completely different from their own. Previously, such phenomena have been mainly discussed from the view-point of pseudologia fantastica or malingering in Japan. The author discusses how a new identity could be developed in cases of generalized amnesia. According to Abeles, et al., generalized amnesia can sometimes serve as psychological suicide. The author emphasizes that the patient's suicidal risk should be evaluated carefully, even if he or she does not seem highly suicidal superficially. Excessive haste to recover from amnesia may heighten the suicidal risk or help develop a distorted personal identity. The principle for the treatment is to exclude an unnecessary therapeutic manipulation and maintain a consistent and comprehensive psychotherapy. The author also discusses factors with which the duration of amnesia can be evaluated in the initial treatment planning. The premorbid personality, the premorbid social adjustment, previous conflicts leading to amnesia, the whole clinical picture of amnesia, the whereabouts of the patient's family, and the suicidal ideation should all be taken into account.
Adult↗
Does an isolated history of loss of consciousness or amnesia predict brain injuries in children after blunt head trauma?
BACKGROUND: A history of loss of consciousness (LOC) is frequently used as an indication for cranial computed tomography (CT) in the emergency department (ED) evaluation of children with blunt head trauma. OBJECTIVE: We sought to determine whether an isolated LOC and/or amnesia is predictive of traumatic brain injury (TBI) in children with blunt head trauma. METHODS: We prospectively enrolled children <18 years old presenting to a level I trauma center ED between July 1998 and September 2001 with blunt head trauma. We evaluated the association of LOC and/or amnesia with 1) TBI identified on CT and 2) TBI requiring acute intervention. We defined the latter by a neurosurgical procedure, antiepileptic medication for >1 week, persistent neurologic deficits, or hospitalization for > or =2 nights. We then investigated the association of LOC and/or amnesia with TBI in those patients without other symptoms or signs of TBI ("isolated" LOC and/or amnesia). RESULTS: Of eligible children, 2043 (77%) were enrolled, 1271 (62%) of whom underwent CT; 1159 (91%) of these 1271 had their LOC and/or amnesia status known. A total of 801 (39%) of the 2043 enrolled children had a documented history of LOC and/or amnesia. Of the 745 with documented LOC and/or amnesia who underwent CT, 70 (9.4%; 95% confidence interval [CI]: 7.4%, 11.7%) had TBI identified on CT versus 11 of 414 (2.7%; 95% CI: 1.3%, 4.7%) without LOC and/or amnesia (difference: 6.7%; 95% CI: 4.1%, 9.3%). Of the 801 children known to have had LOC and/or amnesia (regardless of whether they underwent CT), 77 (9.6%; 95% CI: 7.7%, 11.9%) had TBI requiring acute intervention versus 11 of 1115 (1%; 95% CI: 0.5%, 1.8%) of those without LOC and/or amnesia (difference: 8.6%; 95% CI: 6.5%, 10.7%). For those with an isolated LOC and/or amnesia without other signs or symptoms of TBI, however, 0 of 142 (95% CI: 0%, 2.1%) had TBI identified on CT, and 0 of 164 (95% CI: 0%,1.8%) had TBI requiring acute intervention. CONCLUSIONS: Isolated LOC and/or amnesia, defined by the absence of other clinical findings suggestive of TBI, are not predictive of either TBI on CT or TBI requiring acute intervention. Elimination of an isolated LOC and/or amnesia as an indication for CT may decrease unnecessary CT use in those patients without an appreciable risk of TBI.
Adolescent↗
[A clinical study on the therapeutic significance of classifying total amnesia].
Eight cases of total amnesia were reported. In common to all the cases, there were the definite histories of characteristic situations charged with depressive and isolated mood, although their modes of social adjustment appeared relatively good respectively. Four of the eight cases presented the clinical course of total amnesia as Yamada et al. had previously pointed out. The other four developed total amnesia in peculiar progress and presented rather involved clinical courses. Examining the clinical courses and psychodynamics, the author has suggested that total amnesia would be able to classify two types, such as "simple course type" and "unstable course type". The important difference between two types is as follows. "Simple course type": There were pressing situations after series of actual pending problems such as debts, troubles with a lover and mismanagement in business. Onset of them were reactive under these environmental situations. They presented calm and stable features during partial amnestic period. As the family relations and the actual environments were improved better, they recalled more parts of their personal histories without any difficulty. "Unstable course type": In these cases, the intrapsychic weakness were more important factors than the actual environmental problems. Unlike "simple course type", whenever they recalled some parts of their personal histories, they presented unstable fluctuating features with confusion. Therefore, they needed intensive therapeutic intervention and concern. Generally speaking, total amnesia can be considered not only as defense for the actual conflicts with a repression mechanism but also as "psychologic suicide" which Abeles et al. have mentioned. In addition, emotionally confused evolution in this type may be regarded as exposure of the intrapsychic weakness itself. By the way, the close relationship between total amnesia and suicide has been mentioned in some papers. In this type of total amnesia, attempted suicides were actually seen. So the author has stressed that the risk of suicide should be impressed in the treatment of total amnesia. Among the previously reported cases of total amnesia, in which the clinical courses can be read, 27 cases are "simple course type" and 22 cases are "unstable course type" according to the author's knowledge. And the number of total amnesia has been increasing with the times. So in future, total amnesia may increase in number. The author has emphasized the therapeutic significance of classifying total amnesia. It is useful for the treatment of total amnesia to recognize "unstable course type", in order to foresee the unstable clinical course.(ABSTRACT TRUNCATED AT 400 WORDS)
Adult↗
Amnesia.
Amnesia is a common clinical problem characterized by four features: (1) normal immediate recall, (2) impaired ability to learn, (3) relatively spared ability to retrieve previously learned material, and (4) preserved cognitive and personality characteristics. Amnesia occurs as a distinct mental disorder, and nine variations seen clinically are described here: Korsakoff's psychosis, posttraumatic amnesia, amnesia stroke, postoperative amnesia, postinfectious amnesia, anoxic amnesia, transient global amnesia following ECT, and psychogenic amnesia. The clinical findings which characterize and differentiate these disorders are presented, along with suggestions for management and a discussion of the the outcome of amnesia.
Alcohol Amnestic Disorder↗
[Transient amnesia in the elderly].
The two main aetiologies of transient amnesia in the elderly are idiopathic transient global amnesia (TGA) and iatrogenic or toxic amnesia. Vascular and epileptic amnesia are less common. According to the literature, transient psychogenic amnesia, which is a frequent cause of amnesia at age 30 to 50, is very rare in the elderly. TGA is the prototypical picture of transient amnesia. It occurs more often after age 50, with no identified cause, even if some authors accept emotional stress or minor head trauma as occasional precipitants. The mechanism of TGA remains a matter of discussion. It may be the consequence of a spreading depression similar to that described in migraine with aura, but other arguments support an ischemic mechanism. Iatrogenic amnesias are mainly caused by benzodiazepines (BZs) or anticholinergics. The former may occur in a non-anxious subject, who is not a usual consumer of BZ and takes a single dose. The latter are more often due to a hypersensitivity to anticholinergic drugs, in particular in patients presenting with a covert, incipient Alzheimer's disease. A vascular origin must be considered when amnesia is accompanied by other neurological symptoms, and when the regression of the amnesic disorder is slow, lasting several days. It results from lesions involving various mechanisms and locations, mainly subcortical. Partial seizures, most often mesio-temporal, more rarely frontal, may be the cause of transient amnesia in the elderly, in the absence of a past history of epilepsy. The red flag supportive of an epileptic origin is the repetition of stereotyped amnesic episodes. EEG demonstration of seizures may be difficult and the response to antiepileptic drugs effective on partial seizures is usually good.
Aged↗
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↗
Functional amnesia: clinical description and neuropsychological profile of 10 cases.
We carried out the first neuropsychological study of a series of patients with functional amnesia. We evaluated 10 patients, first with a neurological examination and then with three tests of anterograde amnesia and four tests of retrograde amnesia. Excluding one patient who later admitted to malingering, all patients had a significant premorbid psychiatric history and one or more possible precipitating factors for their amnesia. Eight of the 10 patients still had persistent retrograde amnesia at our last contact with them (median = 14 mo after the onset of amnesia). On tests of anterograde amnesia, the patients performed normally as a group, though some patients scored poorly on tests of verbal memory. On tests of retrograde amnesia, all patients had difficulty re-collecting well-formed autobiographical memories of specific events from their past. In contrast, patients performed as well as controls at distinguishing the names of cities from fictitious city names. On remote memory tests for past public events and famous faces, different patients exhibited different but internally consistent patterns of impaired and spared performance. The variability in the clinical and neuropsychological findings among our patients may be understood by supposing that memory performance is poor in proportion to how directly a test appears to assess a patient's common sense concept of memory. The presentation of patients with functional amnesia is as variable as humankind's concept of what memory is and how it works.
Adult↗
Visual memory-deficit amnesia: a distinct amnesic presentation and etiology.
We describe a form of amnesia, which we have called visual memory-deficit amnesia, that is caused by damage to areas of the visual system that store visual information. Because it is caused by a deficit in access to stored visual material and not by an impaired ability to encode or retrieve new material, it has the otherwise infrequent properties of a more severe retrograde than anterograde amnesia with no temporal gradient in the retrograde amnesia. Of the 11 cases of long-term visual memory loss found in the literature, all had amnesia extending beyond a loss of visual memory, often including a near total loss of pretraumatic episodic memory. Of the 6 cases in which both the severity of retrograde and anterograde amnesia and the temporal gradient of the retrograde amnesia were noted, 4 had a more severe retrograde amnesia with no temporal gradient and 2 had a less severe retrograde amnesia with a temporal gradient.
Amnesia↗
The EEG as a monitor of midazolam amnesia: changes in power and topography as a function of amnesic state.
In order to identify EEG parameters that might be specific for identifying amnesia during midazolam infusion, we examined changes in the EEG power spectrum associated with a period of amnesia, determined by inability to recall a sequence of numbers and objects presented verbally, after intravenous midazolam 0.07 mg/kg in ten normal volunteers. Measurements were taken at baseline, during infusion immediately before and after the onset of amnesia, immediately at end of infusion, and 0.5 and 1.5 h after infusion. All subjects had onset of amnesia during infusion, were completely amnesic by the end of infusion, partially amnesic 0.5 h after infusion, and had complete recall by 1.5 h after infusion. The EEG beta power increased and alpha power decreased during amnesic periods. The beta 1/alpha power ratio was the parameter most specific for amnesia. From a baseline value of 0.20 +/- 0.05 (standard error of the mean [SEM]), it increased to 0.96 +/- 0.26 at the end of infusion and decreased to 0.61 +/- 0.15 0.5 h after infusion. By 1.5 h after infusion, all EEG parameters had returned to baseline values. Beta power changes associated with midazolam amnesia were most pronounced in the Fz and Cz lead positions, and alpha power changes were most pronounced in the Oz position. We conclude that 1) EEG power values, particularly the beta 1/alpha ratio, can identify periods of amnesia after midazolam infusion; 2) specific EEG changes and the presence of amnesia vary with the probable serum concentration of midazolam; and 3) the characteristic EEG pattern during partial or complete amnesia varies as one moves across the cerebral cortex.
Adult↗
Transient epileptic amnesia: a description of the clinical and neuropsychological features in 10 cases and a review of the literature.
OBJECTIVES: To clarify the clinical and neuropsychological aspects of transient epileptic amnesia (TEA) based on 10 personally studied cases as well as review of 21 previously published cases; and to propose tentative diagnostic criteria for the diagnosis of TEA. METHODS: All 10 patients and informants underwent a standardised clinical interview. The radiological and neurophysiological (EEG) data were also reviewed in all cases. The diagnosis of transient epileptic amnesia was made on the basis of the following criteria: (1) there was a history of recurrent witnessed episodes of transient amnesia; (2) cognitive functions other than memory were judged to be intact during typical episodes by a reliable witness; (3) there was evidence for a diagnosis of epilepsy. This evidence was provided by either (a) wake or sleep EEG, or (b) the co-occurrence of other seizure types (if their roughly concurrent onset or close association with episodes of transient amnesia suggested a connection), or (c) a clear cut response to anticonvulsant therapy, or by a combination of these three factors. In addition all patients were administered a comprehensive neuropsychological test battery designed to assess verbal and non-verbal anterograde memory and retrograde memory for famous personalities and personal events. Their results were compared with those of 25 age and IQ matched normal controls. RESULTS: TEA usually begins in later life, with a mean age of 65 years in this series. Episodes are typically brief, lasting less than one hour, and recurrent, with a mean frequency of three a year. Attacks on waking are characteristic. Repetitive questioning occurs commonly during attacks. The anterograde amnesia during episodes is, however, often incomplete so that patients may later be able to "remember not being able to remember". The extent of the retrograde amnesia during attacks varies from days to years. Most patients experience other seizure types compatible with an origin in the temporal lobes, but transient amnesia is the only manifestation of epilepsy in about one third of patients. Epileptiform abnormalities arising from the temporal lobes are most often detected on interictal sleep EEG. Despite normal performance on tests of anterograde memory, many patients complain of persistent interictal disturbance of autobiographical memory, involving a significant but variable loss of recall for salient personal episodes. The epochs affected may predate the onset of epilepsy by many years. CONCLUSIONS: TEA is an identifiable syndrome and comprises episodic transient amnesia with an epileptic basis, without impairment of other aspects of cognitive function. Future studies should consider the question of whether TEA reflects ictal activity or a postictal state, and the mechanism of the persistent autobiographical amnesia. It is hypothesised that the latter may result in part from impairment of very long term memory consolidation as a result of epileptic activity in mesial temporal structures.
Aged↗
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↗
Posttraumatic Amnesia as a predictor of outcome after severe closed head injury. Prospective assessment.
OBJECTIVES: To identify the demographic and clinical variables related to the duration of posttraumatic amnesia after severe closed head injury; to evaluate the usefulness of posttraumatic amnesia duration in predicting outcome at the time of hospital discharge and at 6 months after injury. SETTING: Four clinical centers located in primary care hospitals. PATIENTS: Three hundred fourteen severely injured subjects aged 16 years or older who did not have trauma as a result of a penetrating injury and came out of coma before hospital discharge. INTERVENTIONS: Approximately half of the subjects were administered phenytoin sodium for some period after termination of coma; 17% were administered dexamethasone and 41% morphine sulfate. MAIN OUTCOME MEASURES: Galveston Orientation and Amnesia Test scores defined the duration of posttraumatic amnesia. The Glasgow Outcome Scale was used to grade outcome at the time of hospital discharge and at 6 months. RESULTS: Older age, low initial Glasgow Coma Scale score, nonreactive pupil(s), coma duration, and use of phenytoin were associated with a longer duration of posttraumatic amnesia. Poor pupillary response, time in coma, and duration of posttraumatic amnesia and use of phenytoin was predictive of the 6-month outcome. CONCLUSIONS: The results support the prognostic usefulness of prospectively measuring duration of posttraumatic amnesia after termination of coma. Pending replication, our findings suggest that posttraumatic amnesia duration may be a useful surrogate outcome measure for clinical trials involving interventions for acute head injury.
Adult↗
Cooling-induced retrograde amnesia reflexes Pavlovian conditioning associations in Limax flavus.
The relationships between cooling-induced retrograde amnesia and associations in Pavlovian conditioning in the terrestrial mollusk Limax flavus were studied. In the first experiment, the slugs were conditioned to avoid carrot odor and the experimental conditions required for amnesia induction were studied. Memory reactivation before cooling was found to be necessary for amnesia induction and the induced amnesia was selective for the reactivated memory. In the subsequent experiments, slugs were conditioned to avoid both carrot and cucumber odors using one of three Pavlovian conditioning paradigms, namely two-independent first-order conditioning, phase-2-sequential second-order conditioning and phase-2-simultaneous second-order conditioning, after which amnesia was induced by cooling immediately after presentation of one of the conditioning odors. The amnesia pattern induced differed depending upon the conditioning procedure used, which indicated that amnesia induction was related closely to stimulus associations in slugs. The possible role of cooling-induced retrograde amnesia as a tool for studying memory associations is also discussed.
Amnesia, Retrograde↗
Visual memory loss and autobiographical amnesia: a case study.
Amnesia typically results from trauma to the medial temporal regions that coordinate activation among the disparate areas of cortex that represent the information that make up autobiographical memories. We proposed that amnesia should also result from damage to these regions, particularly regions that subserve long-term visual memory [Rubin, D. C., & Greenberg, D. L. (1998). Visual memory-deficit amnesia: A distinct amnesic presentation and etiology. Proceedings of the National Academy of Sciences of the USA, 95, 5413-5416]. We previously found 11 such cases in the literature, and all 11 had amnesia. We now present a detailed investigation of one of these patients. M.S. suffers from long-term visual memory loss along with some semantic deficits; he also manifests a severe retrograde amnesia and moderate anterograde amnesia. The presentation of his amnesia differs from that of the typical medial-temporal or lateral-temporal amnesic; we suggest that his visual deficits may be contributing to his autobiographical amnesia.
Adult↗
Memory for murder. A psychological perspective on dissociative amnesia in legal contexts.
There is currently a complex and inconsistent state in the law relating to dissociation and dissociative amnesia (McSherry, 1998). Although dissociative amnesia in defendants is relevant to both competency to stand trial and criminal responsibility in principle, courts have typically assumed a skeptical stance toward such claims in practice. However, there is considerable evidence from both nonoffender and offender populations to support the validity of dissociative amnesia in defendants. Further, there is information available to aid in the evaluation of amnesia, such as the quality of the report itself and characteristics of the person reporting the amnesia (e.g., psychopathy). When consideration is given to the legal response to reports of dissociative amnesia by complainants, the situation becomes even more complex. While some courts have rejected recovered memory evidence, others have convicted defendants of historical offenses based on such evidence. In some cases, judges have argued that jurors should be left to decide on the validity of recovered memories based on their common sense and experience. The uncritical acceptance of the validity of repressed memories in complainants by many courts stands in stark contrast to the response to claims of amnesia from defendants. It seems apparent that the courts need better guidelines around the issue of dissociative amnesia in both populations. We think that the increasing scientific understanding of memory in the past decade (see Schacter, 1999) can meaningfully contribute to the development of such guidelines. Responsible, nonpartisan expert testimony from mental health professionals would be one step in the direction of rectifying the current state of law in regards to dissociation.
Amnesia↗