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PubMed1993

Permanent global amnesia with unknown etiology.

Three patients developed severe and selective memory impairment with no known cause, one during a period of a few days and two others during a period of 1 to 2 years. In two of these patients, the amnesia has been stable and circumscribed for 5 to 6 years. The third patient appears to have declined in cognitive functions during the past year, at the age of 78, after 6 years of stable, circumscribed amnesia. Neuropsychological testing reveals severe impairment in the ability to learn verbal and nonverbal material as well as retrograde amnesia covering at least 20 years. CT and routine brain MRIs were uninformative. Subsequently, a high-resolution protocol for imaging human hippocampus with MR revealed that the hippocampal formation was markedly reduced in size in all three patients. The pattern of cognitive impairment and the MR findings are similar to the findings in other patients with chronic amnesia due to a known anoxic or ischemic episode, and differ from the findings in amnesic patients with alcoholic Korsakoff's syndrome. We suggest that the amnesia may be due to ischemic damage to medial temporal lobe brain structures important for memory.

Aged↗
PubMed1999

Interaction of cortex and hippocampus in a model of amnesia and semantic dementia.

We describe a systems-level computational model, called TraceLink, that can explain the major characteristics of the neuropsychology of amnesia and of semantic dementia, a recently discovered syndrome in which there is a progressive loss of semantic memory. It also approximates the normal forgetting curve and presents an explanation of why spaced learning is more efficient than massed learning. A central assumption is that consolidation of memory takes place, probably during dream sleep. The model consists of three systems: trace system (certain parts of the neocortex), link system (includes the hippocampus), and the modulatory system (includes certain basal forebrain nuclei). Lesioning each of these causes a characteristic form of amnesia or semantic dementia. Lesioning the modulatory system causes anterograde amnesia only. Lesioning the link system causes a correlated degree of retrograde and anterograde amnesia. Retrograde amnesia shows the characteristic Ribot curve with relative sparing of remote memories but loss of recent ones. Lesioning the trace system causes semantic dementia. We also review the main sources of constraints for the model and discuss its status and function as well as its falsifiability.

Amnesia↗
PubMed1986

Preliminary validation of a clinical scale for measuring the duration of post-traumatic amnesia.

An operational definition of post-traumatic amnesia is presented and a standardized procedure for the measurement of post-traumatic amnesia, which has been clinically tested in over 100 patients with severe, closed head injury is described. Twenty patients with severe head injuries who were still experiencing post-traumatic amnesia (as defined in this study), were assessed on an independent test of learning ability, as were 20 other patients with severe head injury who were no longer suffering post-traumatic amnesia. The performance of the two groups differed significantly; those in a state of post-traumatic amnesia performed more poorly. Both these groups showed significant impairment when compared with a control group of 20 patients who were in hospital because of orthopaedic injuries that were suffered during a motor vehicle accident. These preliminary results are sufficiently encouraging to recommend this simple procedure for routine use in hospitals, to enhance the accuracy of measuring the severity of head injury. The medicolegal use of this measure is also discussed.

Adult↗
PubMed1975

Duration of amnesia during sedation with diazepam and pentazocine: preliminary report.

Fifteen student volunteers participated in a study to determine the duration of amnesia obtained with diazepam and with pentazocine. The group that received pentazocine experienced only slight sedation and no amnesia. There was extreme variance in the level of sedation and in the incidence and duration of amnesia in the group that received diazepam. When amnesia occurred, it lasted for an average of 24 minutes. All students in the group that received a combination of diazepam and pentazocine were well sedated; the average duration of amnesia was 25 minutes.

Adult↗
PubMed2000

[Amnesia following herpes simplex encephalitis].

We describe three patients presenting themselves with amnesia following herpes simplex encephalitis. All three patients showed anterograde amnesia. Moreover, one patient showed retrograde amnesia extending about fifty years prior to the onset of the illness. Two patients revealed semantic memory disorder, disinhibitory behaviors and confabulations, which suggested the existence of frontal lobe dysfunction. MRI of all three patients disclosed uni- or bilateral temporal lesions. SPECT images showed decreased uptake not only in the temporal lobes but also in the frontal lobes. Amnesia following herpes simplex encephalitis has been thought to be caused by the temporal lobe disorder. However, we postulate that the frontal lobe dysfunction might contribute to the appearance of amnesia.

Aged↗
PubMed2001

Recognizing identical versus similar categorically related common objects: further evidence for degraded gist representations in amnesia.

Studies have shown lower false recognition of semantically related lure words in patients with global amnesia than in matched controls. This pattern has been interpreted as suggesting that medial temporal and diencephalic structures that are damaged in amnesia and that contribute to veridical memory also contribute to false recognition. It has been argued that whereas controls form and retain a well-organized representation of the semantic gist of studied items, patients with amnesia can retain only a degraded gist representation. However, these studies are subject to an alternative interpretation involving greater source confusions in controls. The authors used a categorized-pictures paradigm to test recognition under conditions in which source confusions were unlikely to occur. Relative to controls, patients with amnesia showed reduced false recognition of categorically related pictorial lures, thereby supporting the notion of degraded gist representations in amnesia.

Adult↗
PubMed2001

Impaired delay eyeblink classical conditioning in individuals with anterograde amnesia resulting from anterior communicating artery aneurysm rupture.

Anterior communicating artery (ACoA) aneurysm rupture can lead to an anterograde amnesia syndrome similar to that observed after damage to the hippocampus and medial temporal lobes (MT). It is currently believed that ACoA amnesia results from basal forebrain damage that disrupts hippocampal processing without direct hippocampal damage. Converging evidence from animal studies and computational modeling suggests that qualitative differences may exist in the pattern of memory impairment after basal forebrain or MT damage. For example, animals with basal forebrain but not hippocampal damage are impaired at delay eyeblink classical conditioning (EBCC). In this study, individuals with ACoA amnesia were shown to be impaired at delay EBCC compared with matched controls; this contrasts with the spared delay EBCC previously observed in MT amnesia. This finding suggests the beginning of a possible dissociation between the memory impairments in MT versus ACoA amnesia.

Adult↗
PubMed1992

Equivalent forgetting rates in long-term memory for diencephalic and medial temporal lobe amnesia.

Amnesia can result from damage to either the midline diencephalon or the medial temporal lobe. An important related question has been whether these two forms of amnesia result in similar or different kinds of memory impairment. Earlier studies raised the possibility that differences might exist in the rate of forgetting within long-term memory, specifically, that the forgetting rate is normal in diencephalic amnesia but abnormally rapid in medial temporal lobe amnesia. In the present study, forgetting was studied in five amnesic patients with damage to the medial temporal lobe, six amnesic patients with damage to the diencephalon, and 10 normal subjects. One hundred twenty pictures were presented to the control subjects for 1 sec each and to the amnesic patients for 8 sec each. Retention was then tested after 10 min, 2 hr, and 30-32 hr using four different procedures for testing recognition memory. The different exposure times for the pictures succeeded in matching the performance scores of both groups of amnesic patients and the control subjects at the 10 min retention interval. Both groups of amnesic patients also performed similarly to control subjects at retention delays of 2 hr and 30-32 hr. In addition, performance was nearly identical, regardless whether recognition memory was assessed by asking subjects to select the new items or the old items. The findings emphasize the similarities between medial temporal lobe and diencephalic amnesia.

Aged↗
PubMed1992

Behavioral analysis of internal memory states using cooling-induced retrograde amnesia in Limax flavus.

Temporal evolution of internal memory states in a terrestrial mollusk, Limax flavus, was studied using cooling-induced retrograde amnesia. The slug was conditioned to avoid carrot odor by temporally correlated presentation of carrot juice and a bitter-taste stimulus of quinidine sulfate. We could induce retrograde amnesia by cooling of the conditioned slug immediately after the training trial. Thus, we studied the memory states in the slug using the retrograde amnesia according to strategies used in the studies of memory states in mammals or insects. In the early process of memory acquisition, at least two distinctive memory states were observed, short-term memory and long-term memory (LTM). For LTM, two states were also observed. One was a reactivated state of LTM, which was sensitive to the cooling used to induce the amnesia. The other was a so-called resting state of LTM, which was insensitive to cooling. A few days after memory acquisition, further evolution was observed in that the amnesia could not be induced even if the memory trace was reactivated. The results obtained in Limax flavus was comparable with those obtained in a variety of animals.

Amnesia↗
PubMed2006

[Comparison of retrograde amnesia changes within different injury levels of cerebral concussion in rats].

OBJECTIVE: To investigate the retrograde amnesia changes within different injury levels of cerebral concussion in rats. METHODS: A metallic pendulum striker device of brain injury was deployed to duplicate CC models of different injury levels within Sprague-Dawley (S-D) rats. The investigated animals were divided into two groups according to classification standard, that is, Pure Cerebral Concussion (PCC) group and Complicated Cerebral Concussion (CCC) group. One control group was used, and each group included 8 animals. The retrograde amnesia of each group was assessed by Morris Water Maze (MWM) Test from 3 days preinjury to 7 days postconcussion. RESULTS: Compared with the control group, the retrograde amnesia was detected within 3 days in PCC group, and 5 days in CCC group after injury. At the same time, the two groups both manifested space recognition deficit. CONCLUSION: The retrograde amnesia existed in both pure cerebral concussion group and complicated cerebral concussion. Furthermore, the lasting time of retrograde amnesia in animals correlates to the injury level of brain concussion.

Amnesia, Retrograde↗
PubMed1991

[Transient global amnesia].

Transient global amnesia is a momentary neurological accident frequently encountered in subjects over 50 years of age. Its diagnosis is purely clinical and rests on the sudden occurrence of retention amnesia associated with retrograde amnesia without disturbances in speech or other neurological deficits. The amnesia totally regresses within less than 24 hours. Paraclinical examinations add nothing to the diagnosis. The cause of transient global amnesia is unknown, and the various hypotheses that have been put forward (e.g. epilepsy, transient ischaemia or migraine) have not been confirmed by clinical and epidemiological studies. Despite a low, but real risk of recurrence, the prognosis is perfectly benign, and there is no need for curative or preventive treatment.

Amnesia↗
PubMed1988

Benzodiazepine-induced amnesia and anaesthetic practice: a review.

Anaesthetic practice is the only clinical context in which amnesia is a valued property of benzodiazepine drugs, since decreased recall considerably enhances patient tolerance and acceptance or surgical and diagnostic procedures. Research on the amnesic effects of diazepam, midazolam, lorazepam and flunitrazepam, administered via oral, i.v. or i.m. routes to patients undergoing surgical or diagnostic procedures is reviewed. The degree of anterograde amnesia is a function of the drug, the route of administration and the population of patients being assessed. Retrograde amnesia has not been conclusively demonstrated. Amnesia is more profound for cutaneous-tactile and auditory than for visual stimuli, but actual surgical events, or emotionally laden material, are more likely to be recalled than artificial stimuli. Evidence that the benzodiazepines prevent affective and cognitive processing under general anaesthesia and decrease traumatic postoperative recall of intra-operative events is reviewed. The explanatory value of modern theories of memory for research on benzodiazepine-induced amnesia, and the research potential of the surgical setting are outlined. The development of non-sedative anxiolytics and specific benzodiazepine antagonists provides the tools for assessing the contribution of sedative and anxiolytic properties of drugs to their amnesic effects.

Amnesia↗
PubMed1985

[Effect of TRH and its analog DN-1417 on anoxia-induced amnesia in mice].

The effect of neuropeptides and their analogs on anoxia-induced amnesia was examined using one-trial passive avoidance task in mice. Anoxia, produced by the exposure to CO2 immediately after the acquisition of avoidance response, induced amnesia which is shown by a short latency to enter from the safety compartment into the shocked compartment in the retention test conducted 24 hr later. In these anoxia-treated animals, thyrotropin-releasing hormone (TRH: 10-20 mg/kg), its analog DN-1417 (10-20 mg/kg) and ACTH 4-10 (66 micrograms/body), which were given sc 15-60 min before the retention test, markedly prolonged the latency in a dose-dependent manner, indicating a reversal of the amnesia. Arginine- and lysine-vasopressin also reversed the amnesia at a dose of 100 micrograms/body. These results suggest that TRH and DN-1417, known to reverse the amnesia produced by the protein synthesis inhibitor cycloheximide, have ameliorating effects on the retrieval process of memory.

Adrenocorticotropic Hormone↗
PubMed1983

[Interaction with cholinergic drugs in reversal of cycloheximide-induced amnesia by thyrotropin-releasing hormone and its analog DN-1417 in mice].

The reversal effect of drugs on experimental amnesia was studied using one-trial passive avoidance task in mice. Cycloheximide (120 mg/kg) given sc 30 min before the acquisition of avoidance response caused amnesia by showing short latency to enter from the safety compartment into the shocked compartment in the retention test conducted 24 hours later. In these cycloheximide-treated animals, physostigmine (0.1 mg/kg), thyrotropin-releasing hormone (TRH: 10-20 mg/kg) and DN-1417 (5-20 mg/kg) given sc 15-60 min before the retention test markedly prolonged response latency, indicating reversal of amnesia. The effects of all these drugs were almost completely antagonized by anticholinergic drug, scopolamine (0.4-10 mg/kg). Although physostigmine when administered in conjunction with TRH potentiated the reversal effect, there was no potentiation with DN-1417. Since these drugs did not affect test performance in the cycloheximide-treated mice which had experienced no foot-shock, it is unlikely that the amnesia-reversing effect of the drugs was a result of non-specific suppression on motor activity. These results suggest that cholinergic activation reverses cycloheximide-induced amnesia, and TRH and DN-1417, while they showed a difference in the action of potentiation with physostigmine, may also activate a retrieval process of memory by mediation of cholinergic mechanism.

Amnesia↗
PubMed1994

[Forgetfulness and amnesia: receptor mechanisms and brain mapping].

Inability to remember and amnesia have been shown to be active neurochemical processes. The coupled processes (blockade of the triggering DA stimulating system and activation of the inhibitory GABA-ergic system with the predominant value of postsynaptic D-2 receptors) are a neurochemical basis for development of amnesia. The mechanisms of spontaneous forgetting is provided by a decrease in the activity of the dopaminergic system along with the enhancement of benzodiazepine-GABA-ergic interferentional inhibition. The observed changes in dopamine metabolism, para-tyramine appearance, as well as restructure of D-2 receptors provide the activity of dopamine increasing mechanism which determines the retention of memory traces. A computer model of the spatial interaction of the dopamine membrane-receptor complex was constructed by scanning the samples of synaptic membranes after learning and amnesia. A new method of inducing psychogenic amnesia in human beings has been elaborated. Amnesia is characterized by the absence of increases in the number of cortical connections reflecting the emotional factor of information.

Amnesia↗
PubMed1998

Retrograde amnesia for facts and events: findings from four new cases.

Two patients with presumed hippocampal formation lesions and two patients with more extensive temporal lobe damage, all of whom became amnesic in a known year, were given tests of anterograde and retrograde memory function. The two patients with hippocampal formation lesions had moderately severe anterograde amnesia and limited retrograde amnesia for facts and events that affected, at most, the decade preceding the onset of amnesia. Content analysis could not distinguish the autobiographical recollections of the patients from the recollections of control subjects. The two patients with more extensive temporal lobe damage had severe anterograde amnesia and extensive retrograde memory loss for both facts and events. The results suggest that whether retrograde amnesia is temporally limited or very extensive depends on whether the damage is restricted to the hippocampal formation or also involves additional temporal cortex.

Aged↗
PubMed2004

The dynamic time course of memory recovery in transient global amnesia.

AIMS: To investigate the dynamic time course of transient global amnesia (TGA)--that is, the process of recovery and the interindividual variability--by testing four patients during the day of TGA itself (on three occasions) and at follow up (on two occasions). METHODS: A specially designed protocol focusing on semantic (both conceptual and autobiographical knowledge) and episodic (both anterograde and retrograde components) memory. RESULTS: Every patient showed marked impairment of both anterograde and retrograde episodic memory during the acute phase, with a relative preservation of personal and conceptual semantic knowledge. During the following phase, the authors observed similarities and differences among the patients' patterns of recovery. In general, retrograde amnesia recovered before the anterograde amnesia and anterograde episodic memory was recovered gradually in every case. In contrast, shrinkage of retrograde amnesia was more heterogeneous. In two of the patients, this shrinkage followed a chronological gradient and the most remote events were recovered first. In the two other patients, it depended more on the strength of the trace, and there was no temporal gradient. For the latter, an executive deficit could account for difficulties in accessing both conceptual knowledge and autobiographical memories. CONCLUSIONS: This profile of recovery suggests a "neocortical to medial temporal" process in every case, and the possibility of an additional frontal dysfunction in some cases. Hence, the acute phase seems to be characterised by a common episodic impairment. This variability between subjects appears in the recovery phase with two different patterns of impairment.

Aged↗
PubMed1995

Differential effects of Ketaset/Rompun anesthesia on hypothermia-induced retrograde amnesia and its recovery.

A nonbarbiturate anesthetic consisting of ketamine HCl (Ketaset) and xlyazine (Rompun) was administered to assess the effects of anesthesia on hypothermia-induced retrograde amnesia in Long Evans hooded and Sprague-Dawley albino rats. Results from Experiment 1a indicate that this anesthetic does not attenuate retrograde amnesia, and the findings from Experiment 1b suggest that awakening from Ketaset/Rompun anesthesia at normal body temperature (following administration of deep body cooling) does not attenuate the resulting hypothermia-induced retrograde amnesia. Experiment 2 demonstrated that various delays between training and hypothermia resulted in a temporal gradient that was the same for animals cooled while either conscious or under anesthesia. The results of Experiment 3 showed that rats made amnesic while under anesthesia did not recover the target memory if given a recooling treatment, but rats that were made amnesic while conscious did recover the memory with the same reminder treatment. These findings indicate that the conscious processing of stimuli associated with hypothermia treatment is not necessary in inducing hypothermia-induced retrograde amnesia, but that conscious processing is an important factor if the amnesia is to be recovered with a recooling treatment.

Anesthetics, Dissociative↗