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PubMed1991

Amnesia induced by 2-deoxygalactose in the day-old chick: lateralization of effects in two different one-trial learning tasks.

2-Deoxy-D-galactose, an inhibitor of brain glycoprotein fucosylation, was injected intracranially (10 mumole dose in 10 microliters) into either the left or the right forebrain hemisphere of day-old chicks (Gallus domesticus). Bilateral injection of this dose of 2-deoxy-D-galactose is known to induce amnesia for several learning tasks including one-trial passive avoidance and sickness-induced learning. When a tritiated form of the drug was injected into one forebrain hemisphere only, a significantly large proportion of the dose remained in that hemisphere. Chicks were trained in two different one-trial learning tasks. The first was a passive avoidance task in which the chicks were allowed to peck at a green training stimulus (a small light-emitting diode, LED) coated in the bitter liquid, methylanthranilate, giving rise to a strong disgust response and consequent avoidance of the green stimulus. In the second paradigm the chicks were allowed to peck at a similarly colored dry stimulus but, 30 min later, were injected intraperitoneally with lithium chloride (0.1 ml of 1 M solution), causing a sickness-induced aversion for the green LED. 2-Deoxy-D-galactose caused amnesia for the passive avoidance task when injected before training into the right hemisphere but not the left. However, unilateral injection of the drug before training on the sickness-induced learning task did not cause amnesia. The results indicate that fucosylation of brain glycoproteins is required in the right hemisphere for learning the passive avoidance task but that memory for sickness-induced learning can be retained by either hemisphere.

Age Factors↗

PubMed1990

Anterograde and retrograde amnesia in rats with dorsal hippocampal or dorsomedial thalamic lesions.

The present research was concerned with anterograde and retrograde memory for a socially transmitted food preference in rats with lesions to the dorsal hippocampus or dorsomedial thalamus, and operated controls. In Expt. 1, food-preference training was administered postoperatively and memory was tested following various delays. Both lesioned groups acquired the preference normally, but rats with hippocampal lesions displayed a rapid rate of forgetting that indicated significant anterograde amnesia. In Expt. 2, the food preference was acquired at different times preoperatively and retrograde memory was tested postoperatively. Both lesioned groups exhibited loss of memory when training immediately preceded surgery, but only rats with hippocampal lesions displayed a temporally-graded retrograde amnesia. The results confirmed the differential effects of hippocampal and thalamic lesions on memory performance. It was suggested that memory loss following thalamic lesions was related to factors associated with original learning, whereas the pattern of hippocampal amnesia reflected disruption at a later stage in the learning process.

Animals↗

PubMed1984

Comparison of sedation, amnesia, and patient comfort produced by intravenous and rectal diazepam.

In a cross-over study, intravenous diazepam was compared with rectal diazepam for sedation in outpatient oral surgery. Fifty-four operations were performed on 27 patients. Recovery from sedation, experience during the postoperative course, amnesia, estimation of the sedative effect, and patient preference of method of sedation were studied. The recovery times of the sedation methods did not differ. Sedative effects after the first operation were estimated as good by 87% of patients given intravenous sedation and by 75% of those given rectal sedation. However, there was a significant relationship between the subjective experience of stronger sedative effect and preference of sedation method that favored the intravenous technique. The degree of amnesia was significantly higher during intravenous sedation, but a high degree of amnesia was not related to patients' preference for a sedation method. Neither sedation method produced any local side effects.

Adolescent↗

PubMed1983

The effect of reserpine, syrosingopine, and guanethidine on the retention of discriminated escape reversal: peripherally administered catecholamines cannot reverse the reserpine amnesia in this situation.

In a series of experiments, the effects of reserpine, syrosingopine, and guanethidine on retention of a discriminated escape reversal training were investigated in mice. The peripherally and centrally acting reserpine produced amnesia while the primarily peripherally acting compounds, syrosingopine or guanethidine, did not produce amnesia even when given in high dosages or when training was given with low footshock. Unlike in the passive avoidance situation, peripherally administered norepinephrine or dopamine was not able to attenuate the reserpine-induced amnesia. The results were discussed in terms of the role of biogenic amines in memory formation.

Animals↗

PubMed1988

Strength of scopolamine-induced amnesia as a function of time between training and testing.

Variations in the strength of scopolamine-induced amnesia as a function of age of the habit were studied in Swiss Webster mice. Animals were trained in an active avoidance task to a criterion of 9/10 avoidances and immediately following training injected with scopolamine hydrochloride (1.0 mg/kg) or saline. Retention of the avoidance learning was evaluated by testing different groups of animals 1, 3, 7, 10, 14, and 28 days following training. The retention test consisted of five trials in which the CS but not the UCS was presented. Results indicated that saline-treated mice exhibited near-perfect retention up to 14 days post-training with forgetting beginning to be apparent at 28 days. Scopolamine treatment produced strong amnesia in animals tested 1 and 3 days post-training but normal retention in animals tested 7 and 10 days after learning. The amnesia abruptly reappeared at 14 days after which time it remained stable. The marked similarity of the scopolamine retention curve to changes in the strength of memory of discrimination learning in undertrained rats reported by Deutsch suggested that scopolamine resulted in the storage of a weak memory of the avoidance response. To explore this idea further we trained mice to a criterion (4/5) which would result in a weak avoidance response and tested different groups 1, 3, 10, 14, and 28 days following learning. Results showed that strength of the memory of avoidance learning increased up to 10 days and then decreased abruptly at 14 days thus replicating the general shape of the retention curve produced by injecting scopolamine following strong training. These data suggest that scopolamine disrupts processes essential for the formation of durable memories.

Animals↗

PubMed1999

Midazolam sedation to produce complete amnesia for bronchoscopy: 2 years' experience at a district general hospital.

Patients may find bronchoscopy without sedation unpleasant. There is some evidence that patient satisfaction correlates with amnesia for the procedure. For several years we have used doses of midazolam sufficient to put patients lightly asleep hoping to produce complete amnesia. We looked at practical aspects of this technique over a 2-year period. We studied 337 consecutive patients. They were 219 men and 118 women of mean age 63 +/- 12.4 (SD). Sixty-seven patients were aged 75 years or over and the eldest was 86. Sixty-three patients were already hospital inpatients but the remainder were seen as day cases. Midazolam was given by slow i.v. injection over several minutes until the patient was judged to be lightly asleep. Patients were given supplemental oxygen (3 l min-1) and monitored by ECG and pulse oximetry. A note was made of the time at which they awakened, defined as when nursing staff felt the patients were awake enough to have a cup of tea and toast. Patients were asked if they had any memory of the procedure both on awakening and when seen a few days later to discuss the results. The procedures were carried out in a well-staffed Day Case Unit with a recovery area. The mean dose of midazolam used was 10.8 mg (mean +/- SD = 0.16 +/- 0.095 mg kg-1). The midazolam was given over a median of 4 min (range 1-15 min). Patients took 59 +/- 45 min (mean +/- SD) to wake up. Twenty-eight patients were given flumazanil to reverse the sedation (11 for concern over bleeding following biopsies, three for desaturation during and three after procedure, four as they were frail, two as they were restless, two as they were hypotensive after procedure and three for miscellaneous reasons). Only nine patients could remember any part of the procedure. Incremental doses of midazolam given slowly until patients are lightly asleep almost invariably produce complete amnesia for bronchoscopy. This is a safe technique but patients need careful monitoring and may require reversal of sedation with flumazanil.

Adult↗

PubMed1981

A physiological investigation of volitional and nonvolitional experience during posthypnotic amnesia.

Highly responsive hypnotic subjects, who were classified as having control over remembering (voluntaries) or not having control over remembering (involuntaries) during posthypnotic amnesia, were compared with each other on four physiological measures (heart rate, electrodermal response, respiration rate, muscle tension) during posthypnotic recall. Two contextual conditions were employed: One was meant to create pressure to breach posthypnotic amnesia (lie detector instructions); the other, a relax condition, served as a control. The recall data confirmed earlier findings of Howard and Coe and showed that voluntary subjects under the lie detector condition recalled more than the other three samples that did not differ from each other. However, using another measure of voluntariness showed that both voluntary and involuntary subjects breached under lie detector conditions. Electrodermal response supported the subjects' reports of control in this case. Physiological measures were otherwise insignificant. The results are discussed as they relate to (a) studies attempting to breach posthypnotic amnesia, (b) the voluntary/involuntary classification of subjects, and (c) theories of hypnosis.

Arousal↗

PubMed1984

Intact retention in acute alcohol amnesia.

Research on alcohol amnesia has focused on memory processes that are disrupted during intoxication. The present experiment examined the possibility that certain memory processes might be resistant to the amnesic effects of alcohol. Intoxicated and sober subjects studied a list of 29 words. They were then given one of three different retention tests: free recall, identification of degraded words based on the procedure used by Warrington and Weiskrantz (1970), and yes/no recognition. As expected, free recall was significantly impaired by alcohol intoxication. In contrast, in the identification test, intoxicated subjects benefited to the same degree as sober subjects from prior exposure to the items. The two groups did not differ in immediate recognition memory. The results of the free-recall and identification tasks are similar to findings with chronic amnesic patients and suggest that perceptual fluency is not affected by alcohol, whereas elaborative processes supporting recall are particularly sensitive to disruption during intoxication. The failure to find recognition impairment at the level of intoxication used in this study distinguishes temporary alcohol amnesia from chronic amnesia.

Adult↗

PubMed1993

Childhood amnesia and the beginnings of memory for four early life events.

Childhood amnesia was examined in a between-groups study of adults' memories of 4 datable target events--the birth of a younger sibling, a hospitalization, the death of a family member, and making a family move. College students (N = 222) answered questions about events that had occurred when they were 1, 2, 3, 4, or 5 years old and also about external information sources, such as family stories. Results show that the offset of childhood amnesia (earliest age of recall) is age 2 for hospitalization and sibling birth and 3 for death and move. Thus, some memories are available from earlier in childhood than previous research has suggested. Subjects' mothers judged most of their children's memories as accurate. External information sources were negatively related to recall from the earlier ages (2-3) but positively to recall from later ages (4-5). These results are compatible with a multiple-determinants account of childhood amnesia.

Adult↗

PubMed1994

Retrieval inhibition in directed forgetting and posthypnotic amnesia.

In Experiment 1, subjects received either by word or by list directed forgetting or posthypnotic amnesia instructions. Recall and recognition performance of subjects who received directed forgetting instructions was consistent with previous findings reported by Basden, Basden, and Gargano (1993), with subjects who received by word instructions showing both recall and recognition deficits for to-be-forgotten items. By contrast, subjects who were given by list instructions showed recall but no recognition deficits, which suggests that although differential encoding underlies word method directed forgetting, retrieval inhibition underlies list method directed forgetting. Subjects who received posthypnotic amnesia instructions (irrespective of method of delivery used) showed recall deficits but no recognition deficits, which suggests that retrieval inhibition underlies posthypnotic amnesia. In Experiment 2, recognition scores were lower with public (oral) tests than with private (written) tests, and recovery was equivalent for to-be-forgotten and to-be-remembered items. The results are interpreted as inconsistent with the differential tagging mechanisms proposed by Huesmann, Gruder, and Dorst (1987).

Adult↗

PubMed1977

Respiratory effects and amnesia after premedication with morphine or lorazepam.

Lorazepam, a new benzodiazepine, was compared with morphine for premedication. Ten patients received morphine 10 mg/70 kg i.m. and 10 received lorazepam 4 mg/70 kg i.m. Respiratory effects were assessed from the change in slope (S) and intercept (B) of the carbon dioxide response line, using a development of Read's rebreathing method. Morphine depressed S by 47% (P less than 0.01), but after lorazepam S increased by 27% (P less than 0.05), neither drug altering B significantly. In two volunteers lorazepam was assessed by both the rebreathing and the steady-state methods; after lorazepam S was smaller by the steady-state than by the rebreathing technique. The findings for lorazepam are consistent with the known effects of sleep on carbon dioxide sensitivity. Amnesia lasting 4-8 h occurred in all patients who received lorazepam so that pain and nausea during this period were not recalled, but no patient who received morphine experienced amnesia. We conclude that lorazepam merits further study, particularly where sedation without respiratory depression is needed, as in obstetrics, and where amnesia for uncomfortable procedures is required.

Adolescent↗

PubMed1978

Memory: modification of anisomycin-induced amnesia by stimulants and depressants.

Mice were trained in a passive (foot shock)avoidance task. When administered after training, the stimulants caffeine or nicotine blocked amnesia for the task that had been produced by injections of the protein synthesis inhibitor anisomycin given prior to training. With foot shock at a higher intensity, anisomycin did not produce amnesia by itself, but the administration of the depressants chloral hydrate or sodium phenobarbital after training did cause amnesia. Stimulants and depressants did not have an appreciable influence on the overall degree of protein synthesis inhibition produced by anisomycin. The results support the hypothesis that arousal after training is an important factor in the conversion of short-term to long-term memory.

Animals↗

PubMed1985

Effects of bifemelane hydrochloride (MCI-2016) on experimental amnesia (passive avoidance failure) in rodents.

To further predict the possible activity on memory disorders, the effect of MCI-2016 (bifemelane hydrochloride) was examined using the passive avoidance (PAR) failure technique as an experimental model of amnesia. The amnesia was produced either by post training treatments of electroconvulsive shock (ECS), scopolamine (mice) and cycloheximide or by pre-test injection of scopolamine (rats). In ECS-PAR failure model, the retention test was carried out 3 hr (3 hr experiment) or 24 hr (24 hr experiment) after ECS. MCI-2016 showed a significant improvement when administered just after ECS (3 hr experiment, 30 mg/kg, i.p.) or 0.5 hr before the retention test (24 hr experiment, 10-30 mg/kg, i.p.). Cahopantenate was only active in the 3 hr experiment (500 mg/kg, i.p.), and piracetam was rather active in the 24 hr experiment (60 mg/kg, i.p.). MCI-2016 (30 mg/kg, i.p.) prevented the scopolamine-induced PAR-failure. In this model, physostigmine (0.3 mg/kg, i.p.) exhibited a tendency to improve the failure. In another scopolamine-induced PAR failure model in mice, all of the test drugs showed a significant improvement at different dose levels. The effect of MCI-2016 (25-100 mg/kg, p.o.) was superior to those of piracetam, aniracetam and choline chloride. Higher doses of MCI-2016 were required to improve the cycloheximide-induced PAR failure. Considering the experimental conditions and results, it may be suggested that MCI-2016 ameliorates the amnesia possibly through its influence on memory consolidation and retrieval processes.

Animals↗

PubMed2000

[Korsakoff amnesia syndrome].

PATHOLOGY CORRELATIONS: The Korsakoff syndrome results from cerebral lesions due to thiamine depletion, usually of alcoholic etiology. Other nutritional, or genetic factors, could be implicated. Exceptionally, it results from thalamic disease or a tumor of the third ventricle floor. PATHOPHYSIOLOGICAL CONSIDERATIONS: Anterograde and retrograde aspects of episodic memory are principally impaired, contrasting with the preservation of semantic and procedural memory. Opposition between explicit (impaired) and implicit (unimpaired) memory is one of the main cognitive features of this syndrome. Several cerebral structures, components of various memory systems, are simultaneously damaged. Critical lesion sites for anterograde amnesia involve the memillary bodies, the mamillotalamic tract and the anterior thalamus. Retrograde amnesia is dependent on function abnormalities of a circuit between the dorso-median thalamus and the prefrontal cortex. Impairment of retrieval and chronological disorganization of memories contribute to this extensive retrograde amnesia, probably because of frontal dysfunction. Confabulations and false recognitions are produced in the initial stage of the disease. They are, in the same way, interpreted as the consequence of frontal desafferentation due to dorso-median thalamus damage. The impact of diencephalic destruction on the frontal lobes is evidenced clinically by behavioral changes and dysexecutive syndrome. Neuroimaging studies of the brain show a decreased regional metabolic ration in the frontal areas. PROGNOSIS: Korsakoff syndrome is a serious disorder, responsible for cognitive handicap. There is no curative treatment. Preventive measures, consisting in systematic prescription of thiamine in alcoholics, is the main effective measure.

Aged↗

PubMed1995

A case of bilateral thalamic lesions with anterograde amnesia and impaired implicit memory.

Thalamic nuclei appear to play an important role in memory functioning. Severe anterograde amnesia has been reported with lesions of the dorsomedial and anterior nuclei and their connections. We report the case of a woman with discrete thalamic lesions involving the anterior and dorsomedial nuclei who had a persistent anterograde amnesia. Contrary to a previous case report describing impairment only with explicit memory, this patient had impairment with both implicit and explicit memory. This case is discussed in terms of the relevant literature associating the diencephalon, amnesia, and implicit memory.

Clinical Conference↗

PubMed1979

[Flunitrazepam with anterograde amnesia and reduction of blood pressure before local anaesthesia without intubation in 3000 ENT operations (author's transl)].

After premedication with flunitrazepam=Rohypnol 2 mg orally (2--3 hours preop.) and morphine-atropine (30 min preop.) the patient receives slowly "Ro" i.v. until the phenomenon of volume reduction when speaking is observed. This allows for the smallest possible dosis to achieve sufficient amnesia. After about 20 min the patient becomes responsive again, while his amnesia lasts for about 3 hours more. The cardiovascular functions remain stable with a 25% decrease of systolic blood pressure. Vomiting is reduced. The dry operative field makes microsurgery much easier and improves the final result of the operation. After gaining sufficient experience of the staff, 100% amnesia was achieved in all operations during the last 3 months.

Administration, Oral↗

PubMed1979

Temporal gradients in the retrograde amnesia of patients with alcoholic Korsakoff's disease.

Eleven alcoholic patients with Korsakoff's disease and 15 control subjects were given three tests of retrograde amnesia. The first consisted of photographs of famous faces from the past, the second was a recall test of famous people and events, and the third was a multiple-choice questionnaire. To determine whether previously reported temporal gradients (ie, preservation of remote events) were related to item difficulty, half of the questions dealt with events of transient fame while half concerned subjects that continued to receive public attention for many years. The findings indicate that alcoholic patients with Korsakoff's disease have a marked retrograde amnesia that is characterized by a steep temporal gradient, and that this gradient is not an artifact due to the difficulty of the questions or the method of testing.

Alcohol Amnestic Disorder↗

PubMed1985

Unlike beta-endorphin, dynorphin 1-13 does not cause retrograde amnesia for shuttle avoidance or inhibitory avoidance learning in rats.

Posttraining administration of the opioid peptides, beta-endorphin or the enkephalins, is known to cause retrograde amnesia for a variety of tasks in rats. The present paper studies the effect of the posttraining administration of dynorphin 1-13 on retention of a step-down inhibitory avoidance task and of a shuttle avoidance task. For the purpose of comparison, the effect of human beta-endorphin was also studied. In confirmation of previous results, beta-endorphin (1.0 or 10.0 micrograms/kg, IP) caused retrograde amnesia for the two tasks. Dynorphin 1-13 had no effect at doses between 0.008-125.0 micrograms/kg IP or 1.25-125.0 ng/rat ICV in the inhibitory avoidance task, or at doses of 5.0, 25.0, or 125.0 micrograms/kg in the shuttle avoidance paradigm. These findings suggest that, in contrast to beta-endorphin, dynorphin 1-13 may not be involved in memory regulation at the posttraining period in rats.

Amnesia↗