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PubMed2004

Permanent global amnesia: case report.

PURPOSE: To present a case of permanent global amnesia related to hippocampal damage. Permanent global amnesia is a very rare condition of unknown etiology; lesions restricted to the hippocampus are uncommon, which hinders investigations of this pattern of memory loss. This case is unusually well documented, as the patient underwent extensive neuropsychological evaluations. CLINICAL FEATURES: A cheerful right-handed, 83-year-old retired electrician was first evaluated in 1990 for progressive difficulty in learning new information and in recalling events over the preceding 3-4 years. Tests over the next 5 years showed that the impairment was confined to episodic declarative memory. New verbal information could be stored only in episodic memory in a restricted manner, limited by short-term memory capacity. A relatively mild retrograde amnesia was detected. Semantic and implicit memory was spared, as were other functions evaluated. The patient's language and executive function were strikingly efficient. Magnetic resonance imaging of the brain showed bilateral atrophy of the hippocampi and amygdalae, ruling out conditions such as tumour growth. A diagnosis of permanent global amnesia was made. In the ensuing years, the retrograde amnesia worsened, but no new deficits were identified. CONCLUSION: This case, the first with a detailed cognitive examination, is evidence of a relatively pure hippocampal pattern for memory loss in permanent global amnesia.

Aged↗
PubMedDate not supplied

[Transient global amnesia--possible aetiopathogenetic mechanisms].

Transient global amnesia is a clinically well defined syndrome, characterized by transient isolated epizodes of confusion with inability to acquire new data, repetitive quieries, retrograde amnesia and absence of other neurologic symptoms or signs. Eighteen patients who presented at admission the clinical picture of transient global amnesia were, after the examination, classified in three groups: patients with symptoms or signs of transitory focal ischemia, migraine group, and miscellaneous group. The transitory global amnesia in patients suffering from atherosclerotic changes of the vascular system is usually the first manifestation of transitory ischaemic attack pointing to the vascular insufficiency of the posterior cerebral regions as the cause of attack. The typical transient global amnesia is not a rare phenomenon, but it supposes the existence of the precipitating factors. Although its "pure" form is usually benign, the appearance of other factors such as cerebral neoplasms, involved in the aetiology of transient global amnesia, requires the complete clinical examination of each individual with these symptoms.

Amnesia, Transient Global↗
PubMed1991

Carbon monoxide-induced delayed amnesia, delayed neuronal death and change in acetylcholine concentration in mice.

We investigated the interrelationship of delayed amnesia, delayed neuronal death and changes in acetylcholine concentration induced by carbon monoxide (CO)-exposure in mice. In the test for retention of the passive avoidance task, amnesia was observed 5 and 7 days after CO-exposure when the mice were exposed to CO 1 day after training; in the case when the mice were exposed to CO 5 and 7 days before training, amnesia was also observed in a retention test given 1 day after training. The number of pyramidal cells in the hippocampal CA1 subfield was lower than that of the control 3, 5 and 7 days after CO-exposure. But the neurodegeneration in the parietal cortex, area 1, was not observed until 7 days after CO-exposure. The findings indicated that the amnesia and the neuronal death were produced after a delay when the mice were exposed to CO. In addition, the delayed amnesia was closely related to the delayed neuronal death in the hippocampal CA1 subfield. Moreover, [3H]glutamate and [3H]glycine binding sites did not change after CO-exposure but, 7 days after CO-exposure, the concentration of acetylcholine and the binding of [3H]quinuclidinyl benzilate in the frontal cortex and the striatum were found to have significantly changed, but those in the hippocampus did not show significant change. Therefore, we suggest that delayed amnesia induced by CO-exposure may result from delayed neuronal death in the hippocampal CA1 subfield and dysfunction in the acetylcholinergic neurons, in the frontal cortex, the striatum and/or the hippocampus.

Acetylcholine↗
PubMed2006

Postoperative sedation after major surgery with midazolam or propofol in the ICU: effects on amnesia and anxiety.

BACKGROUND: Propofol and midazolam are commonly used in the ICU to alleviate physical and psychological disturbances in consequence of anxiety. This study was conducted to assess and compare the impact of postoperative sedation after major surgery with midazolam or propofol on amnesia and anxiety in conscious patients under intensive care. METHODS: One hundred and two adult patients irrespective of sex and age, receiving thoracic, abdominal or other major truncal surgery necessitating close care at the ICU, were randomly allocated into midazolam or propofol group. Prior to surgery, all patients were subjected to evaluation of the levels of anxiety and amnesia, which was repeated on the following morning with the level of anxiety and the level of amnesia assessed just before and 30 min after cessation of midazolam or propofol medication, respectively. RESULTS: There were no significant differences between the two groups regarding gender, age, types of analgesics used, and anxiety. In both groups, the levels of anxiety (P < 0.001) and amnesia (P < 0.001) were improved significantly over the following day. Midazolam had more pronounced effects on amnesia than propofol (P < 0.001). There were no significant differences between the two groups in the pre- or post-drug anxiety (P = 0.189). CONCLUSIONS: Both midazolam and propofol are effective amnesic and anxiolytic drugs. Midazolam tends to have more favorable effects on amnesia. It is speculated that combination of propofol and midazolam may give better results for treating critically ill ICU patients, the confirmation of which necessitates further study.

Adult↗
PubMed1978

Conscious sedation with intravenous drugs: a study of amnesia.

A comparison of amnesia that is produced by two intravenous sedation techniques commonly used to reduce anxiety in ambulatory oral surgery patients showed that both techniques induce high levels of safe, predictable amnesia. More than 200 patients undergoing surgical extraction of third molars were asked to verbally identify visual and cutaneous-tactile stimuli intraoperatively. The patients responded via written questionnaires at the postoperative interview sessions. No retrograde amnesia was observed. Complete amnesia was attained for the local anesthetic injections. Amnesia for visual stimuli was significantly lower than for cutaneous-tactile stimuli. No significant differences in amnesia were observed between the two drug combinations studied.

Adult↗
PubMed1986

Human amnesia and the medial temporal region: enduring memory impairment following a bilateral lesion limited to field CA1 of the hippocampus.

During the past 100 years clinical studies of amnesia have linked memory impairment to damage of the hippocampus. Yet the damage in these cases has not usually been confined to the hippocampus, and the status of memory functions has often been based on incomplete neuropsychological information. Thus, the human cases have until now left some uncertainty as to whether lesions limited to the hippocampus are sufficient to cause amnesia. Here we report a case of amnesia in a patient (R.B.) who developed memory impairment following an ischemic episode. During the 5 years until his death, R.B. exhibited marked anterograde amnesia, little if any retrograde amnesia, and showed no signs of cognitive impairment other than memory. Thorough histological examination revealed a circumscribed bilateral lesion involving the entire CA1 field of the hippocampus. Minor pathology was found elsewhere in the brain (e.g., left globus pallidus, right postcentral gyrus, left internal capsule), but the only damage that could be reasonably associated with the memory defect was the lesion in the hippocampus. To our knowledge, this is the first reported case of amnesia following a lesion limited to the hippocampus in which extensive neuropsychological and neuropathological analyses have been carried out.

Amnesia↗
PubMed2006

Amnesia and the hippocampus.

PURPOSE OF REVIEW: Long-term memory impairments have great medical significance and a considerable health and economic burden. Understanding their cognitive and neuroanatomical underpinnings is of crucial importance. Severe amnesia is usually observed following bilateral hippocampal pathology. This review addresses the precise role of the hippocampus and related medial temporal lobe structures in amnesia. RECENT FINDINGS: Disagreements exist over whether, following selective hippocampal damage: retrograde amnesia for episodic memories is temporally limited or extensive and ungraded; anterograde amnesia involves both recollective and familiarity processes. It is accepted that material specific impairments follow unilateral medial temporal lobe damage, with verbal and nonverbal memory lateralized to left or right, respectively. Memory for unknown faces, however, may not depend on the hippocampus. Pharmacological studies in animals, with some extension to humans, highlight promising future therapeutic interventions targeting synaptic plasticity modulation. SUMMARY: Despite considerable progress, some issues remain unresolved. The available evidence favours the view, however, that the hippocampus, in conjunction with other cortical areas, is critical for the retrieval of remote episodic memories and for both recollection and familiarity anterograde memory processes. There are as yet no effective pharmacological treatments for medial temporal lobe amnesia, but various rehabilitative techniques may be useful.

Amnesia↗
PubMed1982

Characteristics of retrograde amnesia following reactivation of memory in mice.

Amnesia for approach-avoidance learning was induced in mice by injecting the protein synthesis inhibitor anisomycin (ANI) immediately, 1, or 2 hours, but not 3 hours after training. A robust amnesia could be demonstrated if ANI was administered 3 hours after training, immediately following a 60 second exposure to the training apparatus or to a structurally similar environment. The temporal gradient of effectiveness of amnesia production by ANI was significantly steeper following reactivation treatment than it was following initial training. In addition, while amnesia produced by the conventional procedure remained stable for 6 days, the amnesia induced following reactivation treatment spontaneously recovered 4 days after training. These findings are discussed in terms of their relevance to interpretations of retrograde amnesia studies.

Animals↗
PubMed1986

Korsakoff's syndrome: a study of the relation between anterograde amnesia and remote memory impairment.

Patients with Korsakoff's syndrome were evaluated with nine tests of new learning ability and three tests of remote memory to determine the correlation between anterograde amnesia and remote memory impairment. There was no correlation between the severity of anterograde amnesia and either the overall severity of remote memory impairment (1940s-1970s) or the impairment observed for more remote time periods (1940s-1950s). However, the correlation between remote memory impairment and anterograde amnesia became progressively stronger with the recency of the time period and was significant for the 1960s-1970s or the 1970s alone. The results support the view that the extensive remote memory impairment in Korsakoff's syndrome is, at least in part, distinct from and unrelated to anterograde amnesia. The more severe impairment observed for more recent time periods could be related to anterograde amnesia in that it reflects anterograde amnesia that was either already in place or progressively developing during recent years. The ability to recall very remote events seems therefore to depend on brain mechanisms distinct from those required for new learning or for recall of more recent events.

Alcohol Amnestic Disorder↗
PubMed1996

Items for assessing posthypnotic recognition amnesia with the HGSHS:A and the SHSS:C.

A procedure for assessing posthypnotic recognition amnesia is described. A set of items for the Harvard Group Scale of Hypnotic Susceptibility, Form A and for the Stanford Hypnotic Susceptibility Scale, Form C were developed and analyzed for reliability and their ability to discriminate individuals who demonstrate posthypnotic amnesia. Recognition amnesia could be assessed as reliably as recall amnesia, and posthypnotic recognition amnesia identified a select subgroup of high hypnotizable individuals who had higher scores on the screening scales. These items may prove useful for assessing posthypnotic recognition amnesia in conjunction with widely used scales of hypnotic susceptibility.

Adult↗
PubMed1988

The relation between lorazepam-induced auditory amnesia and auditory evoked potentials.

We conducted a placebo-controlled double-blind investigation in 15 normal volunteers to study the time course of amnesia to auditory stimulation produced by lorazepam. We also studied the relationship between auditory amnesia and auditory evoked potentials to determine if long-latency auditory evoked potentials (LLAEPs) could be utilized as electrophysiologic predictors of memory. Amnesia was produced by administration of 0.05 mg/kg lorazepam intravenously. To separate the changes in LLAEPs due to generalized sedation from those associated with amnestic properties of a drug, a third group of subjects given 1.5 mg/kg secobarbital was included. Observed frequency and duration of amnesia to auditory stimulation after lorazepam was 58% and 3 hours, respectively (mean values), with marked diminuition of antirecall effect at 120 minutes. Administration of lorazepam increased the latency and decreased the amplitude of N1 and P3 components of LLAEPs. These changes appeared to be a result of generalized sedation rather than the amnestic properties of the drug. We failed to find a definite relationship between amnesia and changes in LLAEPs. We conclude that P3 component of LLAEPs cannot be utilized as an electrophysiologic predictor of amnesia in humans.

Adult↗
PubMed1997

Drugs for amnesia in the ICU.

OBJECTIVE: This review focuses on how patients' recall of their stay in the ICU can be modified pharmacologically. DATA SOURCES: Computerized MEDLINE and PAPERCHASE searches of English- and foreign-language published research from 1966 to 1995, bibliographies, pharmaceutical and personal files, and conference abstract reports. STUDY SELECTION: All abstracts from uncontrolled and controlled clinical trials were reviewed. DATA EXTRACTION: Study design, population, results, and safety information were retained. Efficacy conclusions were drawn from controlled trials. DATA SYNTHESIS: Patients without cerebral injury may recall mental and physical discomfort during their stay in the ICU. All benzodiazepines produce amnestic effects, but the short duration of action, lack of long-acting metabolites, and potent amnestic effects make lorazepam and midazolam preferable in this setting. Infusions of propofol for conscious sedation produce concentrations below those required for consistent amnesia. Opioids generally do not produce amnesia; however, end-organ failure and use of high doses of opioids may increase plasma concentrations to levels that produce impairment of learning and various degrees of amnesia. High infusion rates of ketamine may be required for satisfactory amnesia and pain control (with coadministration of benzodiazepine). Barbiturates and haloperidol do not impair memory in patients who are not critically ill. Antihistamines and anticholinergics that do not penetrate the central nervous system do not produce amnesia. Flumazenil may induce recall. CONCLUSIONS: Patients may remember their stay in the ICU, depending on the type of injury and the drug therapy. Of the drugs presented, benzodiazepines most reliably provide anterograde amnesia, whereas ketamine and propofol exhibit dose-dependent effects on memory.

Aged↗
PubMed1977

Comparative study of retrograde amnesia in rats on active and passive avoidance tasks and spontaneous recovery of memory.

Naive and pretrained rats were trained in two active avoidance paradigms using a pole-climbing box and in a single-trial passive avoidance task using a T-maze. They were then subjected to amnestic treatments with electroshock, leptazol, pentobarbitone, or ether anesthesia. Single retention tests were given at 20-24, 44-48, or 68-96 h posttreatment. Electroshock and leptazol seizures produced retrograde amnesia in all three paradigms, provided that seizures were maximal and retention was tested before 48 h. Prior treatment with anticonvulsant drugs prevented amnesia. Ether and pentobarbitone anesthesia failed to produce amnesia in all three tasks. A trend of recovery from amnesia was observed in the electroshock and leptazol groups when tested for retention 48-96 h posttreatment. On the other hand, the non-amnesic control, pentobarbitone, and ether groups showed signs of forgetting at these longer intervals. Consolidation failure and/or retrieval block was surmised to be the cause of amnesia; recovery was the possible result of removing the block.

Amnesia↗
PubMed1981

Retrograde amnesia produced by electrical stimulation of the amygdala: attenuation with adrenergic antagonists.

Subseizure electrical stimulation of the amygdala produced retrograde amnesia for a visual discrimination shock-motivated task. Animals pretreated with the alpha-adrenergic antagonist phenoxybenzamine, or the beta-adrenergic antagonist propranolol, did not develop amnesia. The findings indicate that adrenergic antagonists attenuate amnesia produced by amygdala stimulation for visual discrimination training. These results are consistent with previous evidence indicating that adrenergic antagonists attenuate the amnesias produced by a variety of agents, and thus, suggest that adrenergic mechanisms may be involved in the production of retrograde amnesia.

Amnesia↗
PubMed1996

A case of simulated, psychogenic or focal pure retrograde amnesia: did an entire life become unconscious?

A case of pure retrograde amnesia following mild head injury is reported. Neuropsychological, psychodynamic and statistical approaches are employed in an attempt to disentangle the clinical picture presented by the patient. Focal retrograde amnesia, psychogenic retrograde amnesia and simulated amnesia are all taken into account. From a public events questionnaire and an inquiry about famous people, consistency analyses showed that the patient was able implicitly to use information she denied having, but at the same time, made us lower the probability of a simulated amnesia. Moreover, psychodynamic analysis showed that the patient's personality structure was compatible with hysterical patterns and we suggest that the patient's memory defect may be related to her personality. It seems less likely, though still possible, that the case may be explained in terms of deliberate simulation. In this case we conclude that the classification along the conscious/unconscious dimension seems more informative than the contrast between psychogenic and organic genesis.

Adult↗
PubMed1984

The effects of somatostatin, its fragments and an analog on electroconvulsive shock-induced amnesia in rats.

In the present study the effects of intracerebroventricularly [icv] administered somatostatin [linear and cyclic], somatostatin3-6, somatostatin7-10 and des AA1,2,4,5,12,13 [D-Trp8] somatostatin [ODT8-SS] were investigated on electroconvulsive shock [ECS]-induced retrograde amnesia in rats. The ECS significantly decreased the foot shock-induced avoidance latency, and thus caused retrograde amnesia. Somatostatin [linear and cyclic] in a dose of 0.6 nM had no action on the ECS-induced retrograde amnesia, while in doses of 3 nM and [cyclic only] 6 nM it significantly prevented it. Somatostatin3-6, somatostatin7-10 and ODT8-SS in doses of 0.6, 3 and 6 nM had no effect on the ECS-induced amnesia. These results indicate that the whole sequence of the original somatostatin molecule is needed to block the ECS-caused retrograde amnesia.

Amnesia↗
PubMedDate not supplied

Long-term amnesia: a review and detailed illustrative case study.

Long-term amnesia is a slowly developing form of anterograde amnesia accompanied by retrograde amnesia of variable severity (Kapur, 1996; 1997) often associated with damage to the anterior temporal neocortex and epileptic seizures. The precise neural and functional deficits that underlie this condition are unknown. A patient, JL, who has this condition following a closed-head injury, is described in detail. Her injury caused bilateral anterior temporal neocortex damage that was more extensive on the left and right-sided damage to the perirhinal and orbitofrontal cortices. The hippocampus appeared to be intact bilaterally. Epilepsy developed within two years of JL's injury. Apart from her memory impairments, JL's cognitive functions, including high-level visual perception, attention, semantic memory and executive functions were well preserved. Her memory also seemed well preserved for at least 30 minutes following encoding. The one exception was the patient's relatively greater impairment at difficult visual recognition tests for which verbalization may not have been an effective strategy. This problem may have been caused by JL's right-sided perirhinal and orbitofrontal cortex damage. Her recall and recognition was clearly impaired after a three-week delay. She also showed a retrograde amnesia, which appeared to be milder than her remote post-morbid memory deficit. JL's remote memory was preserved for information first encountered in either the pre- or post-morbid period provided the information had received sufficient rehearsal over long periods of time. Her long-term amnesia may have been caused by anterior temporal neocortex damage, possibly in association with her epileptic seizures. Whether the condition is heterogeneous, involves a deficit in slow consolidation, disruption of unconsolidated memories, or blockage of maintenance or disruption of insufficiently rehearsed memories whether or not these have been slowly consolidated is discussed.

Adult↗
PubMed1993

Midazolam enhances anterograde but not retrograde amnesia in pediatric patients.

BACKGROUND: Midazolam sedation has been shown to diminish recall of one to four cards shown prior to induction of general anesthesia in pediatric patients. This promising but limited finding prompted us to investigate the effect of midazolam sedation on retrograde and anterograde recall and recognition in children scheduled for elective surgery. METHODS: Forty patients aged 4-10 yr were randomized using a double-blind study design to receive either 0.2 mg/kg intranasal midazolam or 0.2 ml/5 kg placebo (distilled water) using a Devilbiss #286 atomizer. To assess postoperative memory of preoperative events, recall and recognition tasks were performed using a series of picture cards designed for this purpose. Retrograde amnesia was measured by postoperative recall and recognition of cards shown prior to midazolam/placebo administration, and anterograde amnesia was measured by postoperative recall and recognition of cards shown during the interval between midazolam/placebo administration and induction of general anesthesia. RESULTS: Compared to placebo, the midazolam group experienced a significant postoperative reduction in ability to both recall (P < .003) and recognize (P < .001) cards shown subsequent to midazolam/placebo administration (anterograde amnesia). In distinction, there was no difference between groups in postoperative ability to recall or recognize cards shown prior to midazolam/placebo administration (retrograde amnesia). CONCLUSIONS: These results support and extend the inference that midazolam diminishes anterograde recall. In addition, our findings indicate that midazolam diminishes anterograde recognition, thereby providing partial anterograde amnesia without affecting retrograde memory in pediatric patients.

Amnesia↗