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[A case of retrograde amnesia of 22 years, continued for 4 days following a general anesthesia accompanied by a permanent amnesia of these 4 days after the complete recovery from the retrograde amnesia].

A case of global amnesia which continued for 4 days following a general anesthesia and recovered without any neurological deficits was reported. The patient was a 38-year-old woman suspected of lung cancer, and scheduled for pulmonary lobectomy. She had a history of appendectomy under spinal anesthesia 22 years before. She was premedicated with diazepam (10mg), atropine (0.5mg) and pentazocine (30mg). Anesthesia was induced with thiamylal (500mg) and succinylcholine (140mg) iv and 100% oxygen. Anesthesia was maintained with enflurane and nitrous oxide with oxygen for 3 hours. After her recovery from anesthesia, a retrograde amnesia of 22 years was observed and continued for 4 days. Then the memory was restored completely, but the amnesia during these 4 postoperative days remained permanently. We have documented the case of amnesia in the immediate postoperative period which is similar to transient global amnesia. It seems likely that this amnesia was caused by drug interaction, hypoxia, decreased cerebral perfusion or psychogenic effects of general anesthesia.

Adult↗

Recovery of function processes in human amnesia: evidence from transient global amnesia.

There are few clues as to the processes that underlie recovery of function from human amnesia. Evidence is offered from the perspective of a study of recovery of function during an episode of transient global amnesia (TGA) that occurred as a complication of a cerebral angiographic procedure being carried out in a neurosciences centre, and where there was therefore a unique opportunity to examine acute changes in memory function. This allowed us to conduct the first quantitative study where shrinkage of anterograde and retrograde memory loss was plotted at four separate intervals throughout the acute recovery process, and also 24 hr later. Recovery of retrograde amnesia preceded recovery from anterograde amnesia. Resolution of a naming deficit more closely paralleled recovery from retrograde amnesia rather than anterograde amnesia. Within retrograde amnesia for public events, there was a temporal gradient of memory loss, with more recent events affected to a greater degree than earlier events. Within anterograde amnesia, picture recognition memory preceded recovery of story recall memory. On the basis of these findings, and related observations in the published literature, it is proposed that recovery from some types of human amnesia, such as that associated with TGA, follows a 'lateral-to-medial' rule--lateral inferotemporal areas that play a major role in retrograde amnesia recover first from hypometabolism related to the TGA attack, followed by 'interface' areas such as the rhinal and parahippocampal cortices that are considered to have a role in both anterograde and retrograde memory functioning, with the last areas to recover physiological integrity being discrete limbic-diencephalic structures such as the hippocampus.

Adult↗

Amnesia can facilitate memory performance: evidence from a patient with dissociated retrograde amnesia.

A case is reported of a patient who experienced numerous episodes of transient global amnesia (TGA) during which anterograde amnesia was less prominent than usual, and who developed a permanent selective retrograde amnesia. On formal testing, he performed well on traditional verbal memory tests, but showed marked retrograde amnesia for verbal material, including items on a famous voices recognition test. He was administered a paired-associate learning test where the names of famous personalities for which he was amnesic were associated with incongruous activities (e.g. John Newcombe-singing). Our patient performed better on this task than a group of five matched control subjects. Our observations indicate that in the organization of human memory retrograde amnesia may be fractionated from anterograde amnesia and that in certain situations specific types of amnesia can produce a facilitation effect compared to the performance of control subjects.

Aged↗

Transient global amnesia and functional retrograde amnesia: contrasting examples of episodic memory loss.

We studied 11 patients with transient global amnesia (TGA) and ten patients with functional retrograde amnesia (FRA). Patients with TGA had a uniform clinical picture: a severe, relatively isolated amnesic syndrome that started suddenly, persisted for 4-12 h, and then gradually improved to essentially normal over the next 12-24 h. During the episode, the patients had severe anterograde amnesia for verbal and non-verbal material and retrograde amnesia that typically covered at least two decades. Thirty hours to 42 days after the episode, the patients had recovered completely and performed normally on tests of anterograde and retrograde amnesia. By contrast, patients with FRA had a sudden onset of memory problems that were characterized by severe retrograde amnesia without associated anterograde amnesia and with a clinical presentation that otherwise varied considerably. The episodes persisted from several weeks to more than two years, and some of the patients had not recovered at the time of our last contact with them. The uniform clinical picture of TGA and the variable clinical picture of FRA presumably reflect their respective neurologic ('organic') and psychogenic ('non-organic') aetiologies.

Amnesia↗

MK-801 ameliorates delayed amnesia, but potentiates acute amnesia induced by CO.

The effects of non-competitive N-methyl-D-aspartate receptor antagonists on amnesia induced by carbon monoxide (CO) were investigated, since they have neuroprotective effects on delayed degeneration induced by ischemia. In the mice exposed to CO, acute and delayed amnesia were induced. (+)-MK-801 and (-)-MK-801 improved the delayed amnesia, but the effects of phencyclidine (PCP) were weak. (+)-MK-801 and PCP potentiated the acute amnesia. From these results, it is suggested that there is a stereoselectivity in the effects of MK-801 on CO-induced amnesia and that CO-induced delayed amnesia animals could be used as an ischemic amnesia model.

Amnesia↗

Hypnotic amnesia as a strategic enactment: breaching amnesia in highly susceptible subjects.

Hypnotically amnesic subjects frequently maintain their amnesia in the face of strong and repeated exhortations to recall honestly and to try their best to recall. Some investigators have argued that these subjects lose control over memory processes and, consequently, are unable to recall the material for which amnesia had been suggested. We propose instead that amnesic subjects maintain control over their memory processes. They often fail to breach amnesia because to do so would conflict with their self-presentation as deeply hypnotized. In two interrelated experiments we demonstrated that highly susceptible hypnotically amnesic subjects could be easily induced to recall all of the "forgotten" target items by defining successful recall as supportive of rather than as inconsistent with a self-presentation as deeply hypnotized. In the first part of Experiment 1, all subjects showed amnesia despite repeated demands to recall honestly. In the second part of this experiment, subjects were led to believe that they possessed a "hidden part" to their mind that remained aware of the target items covered by the amnesia suggestion. Each subject recalled all of the forgotten items when the experimenter contacted their hidden part. In Experiment 2 we replicated this effect and also demonstrated that the characteristics of subjects' hidden reports were a function of the instructions they received and did not reflect the operation of a dissociated cognitive subsystem that subconsciously held the forgotten items. These findings are inconsistent with traditional theorizing about hypnosis, but offer strong support for the hypothesis that hypnotic amnesia is a strategic enactment under the subject's voluntary control.

Adult↗

Detecting the faking of amnesia: a comparison of the effectiveness of three different techniques for distinguishing simulators from patients with amnesia.

This paper compared the effectiveness of three different procedures that have been put forward as possible ways of distinguishing patients with genuine memory problems from those who are attempting to simulate amnesia. The performance of 20 patients with amnesia was compared with the performance of 20 normal control individuals and 20 normal individuals who had been asked to simulate amnesia on the distraction/no distraction test (Baker, Hanley, Kimmance, & Slade, 1993), the coin-in-the-hand test (Kapur, 1994) and word fragment completion (Horton, Smith, Barghout, & Connolly, 1992). The distraction/no distraction test and the coin-in-the-hand test both proved successful in distinguishing patients with amnesia from simulators (p < .01). Excellent performance by virtually all patients with amnesia coupled with chance or below chance performance by 19/20 simulators on the coin-in-the-hand test was particularly striking. Consistent with the results of Horton et al. ( 1992), the word fragment completion test successfully discriminated between the performance of simulators and controls (p < .01). However, the fragment completion test proved incapable of distinguishing between the performance of patients with amnesia and simulators (p > .05). It is argued that there may be problems inherent in the use of tests designed to investigate implicit memory in attempts to detect malingering.

Adult↗

The relationship between retrograde and anterograde amnesia in patients with typical global amnesia.

An extensive battery of tests of anterograde amnesia and remote memory was given to ten amnesics with lesions either to the medial temporal lobes of the diencephalon. These showed that the patients had anterograde amnesia with deficits in verbal and non-verbal recall and recognition, but preservation of word stem completion and intelligence. Mild impairments on executive tests and digit span performance were largely caused by the poor performance of the Korsakoff patients. The amnesics also showed remote memory deficits for personal and public domain information, and temporal gradients were observed for some of the tests. These deficits probably arose because the patients' anterograde amnesia was more severe than their retrograde amnesia even for the recent pre-morbid past. They were more impaired in the recall of details about famous names in their ability to recognize such names. There was also a suggestion that performance on anterograde tests did not relate strongly to that on tests of retrograde amnesia of the remote pre-morbid past. However, this effect was less apparent with memory for personal information when the format and the information tapped were matched on pre- and post-morbid tests.

Adult↗

Transient global amnesia: evidence for extensive, temporally graded retrograde amnesia.

We gave six patients with transient global amnesia (TGA) neuropsychological tests during and after their episodes. During TGA, all patients had severe anterograde amnesia for verbal and nonverbal material and a patchy but temporally graded retrograde amnesia for personal and public events dating back to at least 1960. In addition, they were unusually passive during TGA, had impaired ability to copy a complex figure, and possibly had mild impairment of confrontation naming. All exhibited complete recovery of memory and other cognitive abilities after the episode. There are similarities between the transient amnesia of patients with TGA and the chronic amnesia of patients with presumed bilateral damage to the medial temporal region or the diencephalic midline.

Amnesia↗

Transient global amnesia or subarachnoid haemorrhage? Clinical and laboratory findings in a particular type of acute global amnesia.

Acute global amnesia may be due to several causes, such as transient global amnesia (TGA), acute drug-related confusional state, toxic substances, metabolic abnormalities, infective diseases, cerebral tumours, cerebrovascular accidents, subarachnoid haemorrhage and epilepsy. In particular both TGA and subarachnoid haemorrhage may be precipitated by sexual activity; by contrast the two diseases are quite different in prognosis and treatment. Ten subjects were admitted in the period 1997-99 to our emergency department for acute global amnesia related to sexual activity. They represented 18% of total acute global amnesias observed in the same period. All patients were males, aged between 41 and 64 years. TGA was found in nine cases, while one patient had subarachnoid haemorrhage, due to rupture of an aneurysm of the right middle cerebral artery. The patient with subarachnoid haemorrhage showed neurologic defects (second-degree nystagmus and retropulsion), while no major neurologic abnormalities were found in TGA. Likewise computerized tomography (CT) scan was positive only in the case of subarachnoid haemorrhage. Patients and relatives in most cases left out sexual activity as a trigger factor. This experience indicates that acute global amnesia related to sexual activity is mostly due to TGA. Major neurologic signs are suggestive of subarachnoid haemorrhage and an immediate CT scan is recommended. Targeted questions are needed to identify the cause of the event.

Adult↗

Posthypnotic amnesia for autobiographical episodes: a laboratory model of functional amnesia?

Extreme variation in the accessibility of autobiographical memory is a major characteristic of functional amnesia. On the basis of its ability to temporarily disrupt the retrieval of memory material, posthypnotic amnesia (PHA) has been proposed as a laboratory analogue of such amnesia. However, most PHA research has focused on relatively simple, nonpersonal information learned during hypnosis. This experiment extended PHA to autobiographical memory by examining high- and low-hypnotizable subjects' explicit and implicit memory of two autobiographical episodes, one of which was targeted by a PHA suggestion. The effects of PHA were consistent with the major features of functional amnesia: PHA disrupted retrieval of autobiographical information, produced a dissociation between implicit and explicit memory, and was reversible. The nature of PHA's effect on autobiographical memory and the potential utility of a PHA paradigm for investigating functional amnesia are discussed.

Adult↗

Is anterograde amnesia a special case of retrograde amnesia?

In anterograde amnesia, memory loss is obtained for events that occur subsequent to the traumatic insult. But because the effects of an anterograde agent or treatment usually last for minutes, or even hours, after the nominal training event, processing of information may be altered during the postacquisition period as well as during acquisition. Since posttraining manipulations are themselves capable of modulating memory, or inducing retrograde amnesia, the memory loss due to a putative anterograde treatment may instead represent retrograde processes. The present experiment examined this potential source of confounding by using an amnestic treatment that can be quickly reversed after training in order to remove postacquisition effects. Thus, the presence of amnesia would isolate anterograde contributions as the source of loss. For induction of anterograde amnesia, rats were trained while at reduced body temperature (29 degrees C). A rapid rewarming procedure was introduced for some animals immediately after training to ensure that the hypothermic state did not extend into the postacquisition period. Other subjects were rapidly rewarmed 1 hr after training to control for any effects of the rewarming manipulation. Both groups showed severe anterograde amnesia that was indistinguishable from that obtained in the gradually rewarmed controls. These data provide an empirical example of an anterograde-induced memory deficit that is independent of retrograde influences.

Animals↗

A comparison between transient amnesias induced by two drugs (diazepam or lorazepam) and amnesia of organic origin.

The transient amnesias produced by drugs may have much in common with the more permanent amnesias associated with organic brain damage. This possibility was investigated using two benzodiazepines, diazepam and lorazepam, with medical student volunteers. In Experiment 1, 27 subjects received a 2ml intravenous injection of either diazepam (7.5 mg) or of lorazepam (3.0 mg) or of normal saline. In Experiment 2, a further 13 subjects were given lorazepam (2.5 mg) or saline. A double blind procedure was used. Neither drug had an appreciable effect on span-type short-term memory (except with 2-channel presentation). Both drugs produced severe anterograde amnesia in other forms of memory test: the amnesic effect of lorazepam lasted for several hours. This amnesia was not attributable to failures of perception. Lorazepam appeared to affect recognition even more than recall. In a test with lorazepam no evidence was obtained that the drug increases susceptibility to proactive interference. With both drugs, recall and recognition were unimpaired of material presented about 10 min before the injection; this shows that the drugs did not affect retrieval mechanisms.

Adult↗

Massive and persistent anterograde amnesia in the absence of detectable brain damage: anterograde psychogenic amnesia or gross reduction in sustained effort?

The case of a young patient with severe and persistent anterograde amnesia of no known cause is reported. Anterograde amnesia arose within a 1-month period and has persisted for more than 1 year. Although a wide variety of neurological and neuroradiological assessments were completed (EEG, evoked potential recordings, Doppler sonography, MRI, PET), no evidence of brain damage was detected. Neuropsychologically, the patient was of high intelligence, had average to above-average short-term memory, and normal retrograde memory abilities, but severe and persistent anterograde amnesia in both verbal and nonverbal domains. Furthermore, he demonstrated grossly reduced long-term concentration. It is likely that a complex chain of interacting variables can produce a syndrome that appears phenomenologically as anterograde amnesia without organically measurable correlates.

Adult↗

Two cases of transient partial amnesia in the course of transient global amnesia.

In the course of transient global amnesia, two patients showed symptoms of transient partial amnesia. Close observation showed that at some time during the episode the patients had some degree of nonverbal memory, which recovered earlier than verbal memory. Careful observation of the progression of symptoms during an episode of transient global amnesia may often reveal symptoms of transient partial amnesia.

Amnesia↗

The effects of repeating a recognition test in lorazepam-induced amnesia: evidence for impaired contextual memory as a cause of amnesia.

In two experiments, a recognition test for an earlier presented list was given twice in immediate succession (Test 1 and Test 2). On the hypothesis that anterograde amnesia for episodic memory involves a deficit in contextual memory, amnesic subjects should confuse familiarity with distractor items gained during Test 1 with familiarity gained during original list presentation. As a result, they should think that they recognize more items on Test 2. This will lower recognition efficiency in Test 2 by increasing false alarms rather than by reducing hits. For subjects with an amnesia induced by lorazepam, but not for control subjects, recognition efficiency was substantially reduced in Test 2 in both experiments. As predicted, this impairment was due to a large increase in false alarms, with no decrease in the number of hits. The impairment could not be explained by a difference in recognition level between lorazepam and control subjects on Test 1. These findings therefore support the contextual memory deficit hypothesis of anterograde amnesia. Their implications for understanding the relationship between recall and recognition in amnesia are discussed.

Adult↗

Amnesia attenuation specificity: propranolol reverses norepinephrine but not cycloheximide-induced amnesia.

Post-trial injections of norepinephrine (NE) or cycloheximide (CHX) into the amygdala produces a long-term retention deficity (amnesia) for a 1-trial footshock experience in rats. concomitant post-trial injections of the adrenergic antagonist, propranolol, prevents NE-, but not CHX-induced amnesia. These results indicate separate mechanisms of action for amnesia produced by intracranial CHX and NE injections.

Amnesia↗