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PubMed1980

The effects of context and subjects' perceived control in breaching posthypnotic amnesia.

Subjects selected on the basis of being amnesic and experiencing their amnesia as "voluntary" or "involuntary" were subjected to two conditions designed to breach their amnesia: (1) lie detector, and (2) honesty instructions. A third group receiving relaxation instructions served as a control. Posthypnotic amnesia was breached under lie detection and honesty conditions. However, there appeared to be an interaction between how subjects reported their experience of amnesia (voluntary and involuntary) and the degree to which amnesia was breached. Voluntary subjects accounted for the majority of breaching. Implications for (1) studies on breaching (2) theories and processes of posthypnotic amnesia, and (3) studies in posthypnotic amnesia are discussed.

Amnesia↗
PubMed1987

Amnesia: organic and psychogenic.

This paper describes the clinical features of selected examples of organic and psychogenic amnesia, and it discusses the nature of the dysfunction that these amnesias entail. The anterograde component of organic amnesia involves a severe impairment in acquiring (or learning) new information, rather than accelerated forgetting, and this may reflect an underlying limbic or neurochemical dysfunction. Retrograde amnesia has a basis which is (at least partially) independent of anterograde amnesia--in some patients, it appears to involve a failure to reconstruct past experience from contextual cues, and this may reflect a super-imposed frontal dysfunction. Two types of confabulation are discussed, one of which ('provoked') is a normal response to poor memory, and the other ('spontaneous') appears to reflect incoherent, context-free retrieval, associated with more severe frontal pathology. It is argued that many cases of psychogenic amnesia may resemble organic amnesia, in that they result from an impaired acquisition of information at the time of initial input, perhaps thereby predisposing the subject to subsequent retrieval difficulties.

Amnesia↗
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↗
PubMed1988

[Effect of naftidrofuryl oxalate (LS-121) on experimental amnesia model in rats].

Effects of naftidrofuryl oxalate (LS-121) on experimental amnesia models, which were induced by cycloheximide (CXM), scopolamine (SCOP) and basal-forebrain (BF) lesion, were investigated using the step-through passive avoidance response in rats. In the retention test, a cut-off time of 600 sec was employed for the measurement of step-through latency (STL). The animals, that showed over 300 sec of STL was regarded as having the criterion of memory retention (% of retention). Increase in both parameters of STL and % of retention was regarded to indicate that the drug was able to improve the amnesia. If only one of the two parameters was increased, we considered that the drug had a tendency to improve the amnesia. Pretraining, post-training and pre-retention treatment of LS-121 (25 mg/kg) improved CXM- and SCOP-induced amnesia. Post-training treatment of LS-121 (25 mg/kg) showed a tendency to improve the BF lesion-induced amnesia. These results suggest that the antiamnesic action of LS-121 may be produced through an activation of the acetylcholinergic neuronal system. Since it improved the amnesia when administered in the pre-retention test, there is a possibility that LS-121 has not only a protective effect, but also a therapeutic effect. Furthermore, it is suggested that LS-121 may also have a therapeutic effect on Alzheimer's disease, since it showed a tendency to improve the BF lesion-induced amnesia.

Amnesia↗
PubMed2001

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

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

Accidents, Traffic↗
PubMed2004

[Changes in visual event-related potentials and SPECT in dissociative amnesia].

A 29-year-old man was admitted because of sudden onset of retrograde amnesia. The patient was unable to recall events having occurred during the past 2 years. The impairment was especially serious with regard to personal memories during the 5 months prior to admission, while he had first been working as a full-time employee under stressful circumstance. A diagnosis of dissociative amnesia was made on the basis of absence of any systemic or neurological diseases that could cause amnesia, the inadaptable character of the patient, the nature of amnesia, and presence of stressful condition possibly related to the amnesia. Visual event-related potential (ERP) studies recorded with human face discrimination tasks demonstrated a P3a wave in response to a face of his superior in the office, whom he said that he had never seen before. The similar P3a wave was observed in response to a face quite familiar to the patient, his mother, but not to a face "truly" unknown to him. These findings suggest that the visual memory of his superior's face exists in the brain, but the patient is unable to retrieve it by some psychogenic mechanism. 131I-IMP SPECT revealed decreased perfusion in the left medial temporal lobe and the basal forebrain, suggesting the association between dissociative amnesia and focal brain dysfunction. While dissociative amnesia has been understood as psychogenic nature, both ERPs and SPECT are quite important tools to understand the association between the psychological phenomenon and biological changes of the brain in this disorder.

Adult↗
PubMedDate not supplied

[Transient global amnesia (a study of 30 cases)].

The authors have studied 30 patients with transient global amnesia aged between 49 and 76 years (median age of 63 years), without focal neurologic signs that have been followed for periods varying between 6 months and 10 years. Three of the patients had recurrent attacks of transient global amnesia, and another three had a stroke, although at some distance from the amnesia attack. Association was noted with certain risk factors including high blood pressure, and angiopathic changes of the eye fundus (in 50% of the patients), dyslipidemia (in 30%), diabetes (in 10%), and essential polyglobulia (in 7%). Coagulation studies including thrombelastograms were carried out in 22 patients, and demonstrated hypercoagulability in 50% of them. Changes in the arterial wall were noted in 85% of the 14 patients in whom carotid sphygmograms were recorded. The presence of these risk factors could explain the occurrence of cerebrovascular accidents in patients with transient global amnesia. Electroencephalograms performed immediately or a short time after the amnesia attack have evidenced in 18 patients rapid-type dysrhythmia, or diffuse theta waves, predominantly located in the deep layers of the left and right temporal areas. The EEG tracings were either flat or normal in the remaining 12 patients. Of the 30 patients presenting with global transient amnesia only two had migraine in antecedents, and another six had headache during the evolution of amnesia. The neurologic examination did not reveal any abnormality in 27 of the patients. Sequelar signs of neurological deficits were noted in the remaining three patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1982

Episodic and semantic memory in posthypnotic amnesia: A reevaluation.

Recently, Kihlstrom found that a suggestion for posthypnotic amnesia produced impairments on episodic but not semantic memory tasks. During amnesia testing, highly and very highly susceptible subjects showed reduced recall for a previously learned word list but no deficits on a word association task designed to elicit the forgotten words as associates. He hypnotized that posthypnotic amnesia involved a dissociation between episodic and semantic components of memory. We tested the alternative hypothesis that Kihlstrom's findings resulted from experimental demands conveyed by the wording of the amnesia suggestion he employed. We found that subjects could be induced to show only episodic impairments (thereby replicating Kihlstrom) or both episodic and semantic impairments (contrary to Kihlstrom) by subtly varying the wording of amnesia suggestions. These findings are inconsistent with a dissociation hypothesis. Instead, they support the notion that hypnotic amnesia is a strategic enactment strongly influenced by expectations generated in the amnesia testing situation.

Adult↗
PubMed1980

Effects of social-physiological variables on hypnotic amnesia.

Three experiments assessed the hypothesis that suggested amnesia for a previously learned word list is a function of subjects' interpretations of the ambigous aspects of the amnesia testing situation. By manipulating preliminary instructions concerning interpretations of this situation, subjects who were unselected with respect to hypnotic susceptibility were induced to show either substantial increments or decrements in amnesia. However, subjects high on hypnotic susceptibility ignored preliminary instructions and therefore could not be induced to show decrements in amnesia. Previous findings of more amnesia in hypnotic than in task-motivated subjects were both replicated and reversed by varying subjects' interpretations of the amnesia task. Analyses on the combined data from the three experiments confirmed earlier findings that partial amnesics tend to recall list items in a relatively disorganized fashion. All of these findings are consistent with an inattention hypothesis of suggested amnesia. Theoretical implications for hypnosis research are discussed.

Adolescent↗
PubMed2004

[Primary loss of consciousness and amnesia in subarachnoid hemorrhage--a quantitative study].

Subarachnoid hemorrhages (SAH) being sudden events affecting the brain in a rather wide-spread fashion are apt to induce loss of consciousness (LOC) and amnesia. The aim of the present study was to collect data on their frequency and extent. To this end we examined 48 patients at a mean of one year post-onset. Two thirds of them reported anterograde and an additional 17% retrograde amnesia; in 40% LOC (median 6 minutes) was observed. The durations were extremely skewed towards shorter times with a median of 2.7 days for anterograde and 1.3 days for retrograde amnesia who--with a single exception--were markedly shorter than anterograde amnesia. Summing up, a significant proportion of all SAH suffered LOC and amnesia occurred in the majority of cases. SAH therefore are events which with respect to LOC and amnesia bear some resemblance with closed head injuries. Exact observation and history taking may disclose important data on their severity and possible sequelae.

Adult↗
PubMed1987

The incidence of awareness, and amnesia for perioperative events, after cardiac surgery with lorazepam and fentanyl anesthesia.

One hundred patients (mean age 59 +/- 10 years) were premedicated with morphine, 0.15 mg/kg, and scopolamine, 0.008 mg/kg. Anesthesia was induced with lorazepam, 50 microg/kg, followed by fentanyl, 50 microg/kg, oxygen and pancuronium, 0.15 mg/kg. Isoflurane was given for short periods before and after cardiopulmonary bypass to 57 patients when hypertension was uncontrolled by addition of fentanyl and/or nitroglycerin. Morphine was used as the sole sedative postoperatively. Patients were interviewed following discharge from the surgical intensive care unit to assess the incidence of operative awareness, and to assess amnesia for events occurring during four preoperative and two postoperative periods of the patients' hospital stay. During three preoperative periods (day of admission, evening before, and morning before operation), 1%, 3%, and 2% of patients had complete amnesia, and 19%, 41%, and 31% had partial amnesia of events. Fifty-five percent of patients exhibited complete, and 34% of patients exhibited partial amnesia to events occurring in the preinduction period. Two patients reported intraoperative awareness (noises, conversation) occurring at the end of the anesthetic. In the two postoperative periods (morning of the day after surgery and intensive care stay), 9% and 15% of patients had complete, and 35% and 47% of patients exhibited partial amnesia. Amnesia was statistically significantly greater in patients over 60 years of age in the preinduction period. Duration of cardiopulmonary bypass did not affect the incidence of amnesia.

Aged↗
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↗
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↗
PubMed1981

[Amnesia and closed craniocerebral injury. A clinical study of 82 cases].

In this investigation 82 patients with various head traumas are examined with respect to time and duration of retrograde, congrade and anterograde amnesia, especially the dependence of their duration on the severity of trauma. The more severe the trauma, the longer the duration of all forms of amnesia, the retrograde being the shorter whether there is a loss of conscience (congrade amnesia) or not. A tendency of amnesias to shrink could only be examined following mild brain trauma and occurred seldom. Our findings suggest that short amnesias have less tendency to shrink than long ones. The distribution of amnesias support cybernetic memory models. As a consequence of our findings we give recommendations for the clinical evaluation of patients with head-brain trauma.

Adolescent↗
PubMed2002

Unexplained sudden amnesia.

BACKGROUND: In almost all cases of acute, sudden, persistent amnesia, the cause can be determined. Ischemic stroke, hypoglycemia, syncope, and seizure are the most likely causes. PATIENTS AND METHODS: In a clinical study, 2 elderly men are described in which sudden, permanent amnesia developed in the absence of a satisfactory explanation. In 1 case, a neuropathologic study disclosed Alzheimer disease; in the other, magnetic resonance imaging showed a temporal lobe abnormality bilaterally. RESULTS: A man aged 80 years suddenly lost his memory of the previous 60 years. Neuropathologic study 5 years later showed the changes of Alzheimer disease. In the second case a disabling amnesia developed overnight in a man aged 70 years. There was no progression of the disabling amnesia in the next 15 years. Magnetic resonance imaging 10 years from the onset showed abnormality of the medial temporal lobe bilaterally. CONCLUSIONS: In neither case was the amnesia satisfactorily explained. It is likely that rare cases of amnesia occur as the result of an unrecognized pathophysiologic process.

Acute Disease↗
PubMed1996

TraceLink: a model of amnesia and consolidation of memory.

A model of amnesia is introduced, called TraceLink, that consists of three systems: 1) a trace system (neocortex), 2) a link system (hippocampus), and 3) a modulatory system (hippocampus/fornix/basal forebrain). It aims to explain salient aspects of the neuropsychology of amnesia, such as Ribot gradients in retrograde amnesia, patterns of dissociation between anterograde and retrograde amnesia, recovery from amnesia, and a newly discovered form of amnesia (semantic dementia) that results from certain temporal lobe lesions that do not affect the hippocampus. The model, furthermore, offers a new explanation for the global neuroanatomy of the hippocampus and neocortex based on the assumption that the brain aims to minimize connectivity volume. It also offers various strategies for the consolidation of memory, the effects of which are explored in computer simulations. The paper concludes with ten, largely untested; predictions derived from the TraceLink model.

Amnesia, Retrograde↗
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↗
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↗