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PubMed1966

Anticholinesterase-induced amnesia and its temporal aspects.

Injection of the anticholinesterase drug diisopropyl fluorophosphate into the hippocampi of rats, 30 minutes after escape learning, produces partial amnesia with full recovery 5 days after injection. No such amnesia is produced if the injection takes place 3 days after learning. However, with injections 5 days after learning there is again an effect, and at 14 days amnesia is complete though no normal forgetting occurs within this period.

Amnesia↗
PubMed1966

Long temporal gradient of retrograde amnesia for a well-discriminated stimulus.

This experiment tested the general validity of recent findings that retrograde amnesia can be produced by electroconvulsive shock only if the shock is administered within 10 to 30 seconds after the learning trial. Precautions were taken to avoid confusion of other shock effects with retrograde amnesia. A temporal gradient of elec- troconvulsive shock-produced retrograde amnesia, extending up to at least 1 hour, for a well-discriminated stimulus, was demonstrated in mice in a one-trial learning passive avoidance situation.

Amnesia↗
PubMed1967

Retrograde amnesia produced by intraperitoneal injection of physostigmine.

Intraperitoneal injection of physostigmine in rats produced a retrograde amnesia of a trained task of escaping shock. This amnesic effect was a U-shaped function of the length of the interval between initial training and injection. In all cases, retraining Occurred 30 minutes after injection. A substantial effect was produced by physostigmine if its application was made 30 minutes after training; there was no effect if application and tests were made 1, 2, or 3 days after the original training. When the substance was injected and the rats were retrained 5, 7, or 14 days after the original training, a substantial effect again appeared. These results are similar to those reported in experiments in which another anticholinesterase, diisopropyl fluorophosphate, was applied intracerebrally. The data demonstrate a similar pattern of change of the amnesia with time, and they substantiate the view that neither the place of application nor the brain lesions caused the reported amnesia.

Amnesia↗
PubMed1968

Amnesia: a function of the temporal relation of footshock to electroconvulsive shock.

When rats received a brief footshock upon stepping off an elevated platform, and an electroconvulsive shock 30 seconds or 6 hours afterward, amnesia was not observed 24 hours later. If a second footshock (noncontingent) was delivered 0.5 second before the electroconvulsive shock, amnesia was observed. The amnesia was temporary if conditioning was strong and permanent if conditioning was weak.

Amnesia↗
PubMed1973

Differential diagnosis of transient amnesia.

In a group of 39 consecutive patients attending neurological clinics with transient amnesia patients with transient global amnesia formed the largest group; others suffered from epilepsy, migraine, temporal lobe encephalitis, or psychogenic fugues. In most cases the clinical features suggested the aetiology, but an electroencephalogram recorded as soon after the attack as possible may help in distinguishing amnesia due to temporal lobe epilepsy.

Adolescent↗
PubMed2006

Prospective comparison of acute confusion severity with duration of post-traumatic amnesia in predicting employment outcome after traumatic brain injury.

BACKGROUND: Measurement of the duration of post-traumatic amnesia (PTA) is common practice, serving as an important index of the severity of traumatic brain injury (TBI) and a predictor of functional outcome. However, controversy exists regarding the nature of PTA; some studies indicate that it is a confusional state with symptoms that extend beyond disorientation and amnesia. OBJECTIVE: To evaluate the contribution of the severity of acute confusion 1 month after TBI to prediction of employment at 1 year after injury, comparing it with PTA duration. METHODS: Prospective study involving 171 participants with complete data, who met the study criteria, from 228 consecutive TBI Model System admissions. Outcome measures included weekly administration of the Delirium Rating Scale-Revised-98 (DelRS-R98) to measure the severity of acute confusion. Evaluations closest to 1 month after injury were used for study purposes. Duration of PTA was defined as the interval from injury until two consecutive Galveston Orientation and Amnesia Test scores of > or = 76 were obtained within a period of 24-72 h. Univariable and multivariable logistic regression were used to predict employment status at 1 year after injury. RESULTS: Age, education and DelRS-R98 were significant predictors accounting for 34% of outcome variance. Individuals with greater confusion severity at 1 month after injury, older age and lower levels of education were less likely to be employed at 1 year after injury. Severity of confusion was more strongly associated with employment outcome (r(s) = -0.39) than was PTA duration (r(s) = -0.34). CONCLUSIONS: In addition to demographic indices, severity of acute confusion makes a unique contribution to predicting late outcome after TBI.

Acute Disease↗
PubMed1982

Are hippocampal lesions sufficient to cause lasting amnesia?

A 57-year-old woman developed severe generalised amnesia following an embolic stroke. The amnesia persisted until her death nine months later. The left hemisphere had a large infarction of the medial temporal-occipital region, while the right showed only a small infarct limited to the posterior two-thirds of the hippocampus. If bilateral lesions are necessary for the production of permanent amnesia, the findings support the view that the hippocampus is itself a critical structure in the medial temporal diencephalic memory circuit.

Amnesia↗
PubMed1983

Amnesia following the rupture and repair of an anterior communicating artery aneurysm.

Clinical analysis and neuropsychological criteria derived from experimental studies of human amnesic syndromes, particularly the alcoholic Korsakoff's syndrome, have been used to characterise an unusual form of amnesia that occurred in two patients after rupture of an anterior communication cerebral artery aneurysm. Intraoperative observation and multiple CT scans did not reveal focal brain damage. Arteriography showed that both patients had arterial vasospasm. The amnesia has persisted over three years since the surgery. Study of the characteristics of their amnesia showed several features in common with other amnesic syndromes, including severely depressed free recall, and less depressed recognition of visual and verbal material. Chronic amnesic syndromes with characteristics of classical amnesic syndromes occur infrequently after rupture and repair of intracranial aneurysms, and, if not caused by parenchymal haemorrhage, may follow pre-operative vasospasm.

Adult↗
PubMed1996

Assessment of post-traumatic amnesia after severe closed head injury: retrospective or prospective?

BACKGROUND: Post-traumatic amnesia is considered to be the best single indicator of the severity of closed head injury. Usually, it has been estimated retrospectively. For practical reasons this also tends to be the most common clinical method. It has been argued that prospective assessment is more accurate and reliable, but this has never been evaluated empirically in severe head injury. METHODS: Post-traumatic amnesia was initially assessed prospectively and later retrospectively by a separate observer in the same patients. RESULTS: The correlation between the two methods was high. In addition, both measures significantly correlated with other measures of severity of brain injury and with measures of outcome. CONCLUSION: Retrospective measurement of post-traumatic amnesia is a valid method.

Adolescent↗
PubMed1998

Amnesia after a discrete basal forebrain lesion.

Destructive lesions of the basal forebrain are often associated with memory impairment and this structure is thought to contribute to memory function by providing a cholinergic input to critical structures associated with memory such as the hippocampus and amygdala. In previously reported cases of amnesia associated with damage in the basal forebrain, multiple neuroanatomical regions were damaged, and the critical lesion responsible for amnesia has not been identified clearly. We report a patient who developed primarily anterograde amnesia after clipping of an unruptured anterior communicating artery aneurysm. Postoperative magnetic resonance imaging showed a discrete lesion, centering in the right diagonal band of Broca and including the anterior hypothalamus, septal nucleus, lamina terminalis, and paraterminal gyrus, and an indiscrete patchy lesion in the corresponding area on the opposite side. The nucleus basalis of Meynert was minimally affected and the diencephalon was not damaged. Single photon emission computed tomography showed marked hypoperfusion in the midline frontobasal region corresponding to the MRI lesion and hypoperfusion in the hippocampus bilaterally. It is concluded that disconnection of the pathway between the diagonal band of Broca and the hippocampus contributed to memory impairment.

Amnesia↗
PubMed2003

A case of frontal network amnesia.

A 63 year old man developed an amnesic syndrome coupled with an array of "frontal lobe" signs after bilateral small subcortical infarcts. His amnesia was characterised by severe difficulty in voluntary recall of recently memorised verbal and non-verbal materials, while his recognition for the same materials was less affected. The symptoms remained unimproved at a follow up evaluation eight months after onset. Magnetic resonance imaging showed two small circumscribed lesions, one in the dorsomedial nucleus of the left thalamus and the other in a region of the right globus pallidus and anterior limb of the right internal capsule. The mammillothalamic tracts and anterior nuclei of the thalami were clearly spared bilaterally. The left dorsomedial nucleus lesion disrupted the thalamofrontal circuit, while the anterior limb lesion of the right internal capsule disconnected the same circuit by damaging part of the anterior thalamic radiation. Thus the amnesia in this patient may have been caused by disruption of the bilateral thalamofrontal circuits. This type of amnesic pathology should be separated from more conventional types of amnesia that are produced by disruption of the so called Papez circuit or the Delay-Brion memory system.

Amnesia↗
PubMed1998

Effects of Jen-San-Yaung-Jung-Tang on scopolamine-induced amnesia in rats.

The effect of Jen-San-Yaung-Jung-Tang (YJT) on scopolamine (SCOP)-induced amnesia was investigated in a step-through passive avoidance task in rats. It was observed that YJT (0.5 and 1.0 g/kg) significantly improved SCOP-induced amnesia and did not change the horizontal activity and pain threshold. YJT at 0.5 and 1.0 g/kg also did not change SCOP-treated horizontal activity and pain threshold. Furthermore, the antiamnesic effect of YJT at 1.0 g/kg on the SCOP-induced amnesia was augmented by physostigmine, but was not altered by neostigmine or scopolamine N-methylbromide. These results suggest that the antiamnesic effect of YJT could only be related to the memory-related process, and to an increase in central cholinergic neuronal activity.

Amnesia↗
PubMed1988

Transient global amnesia and stroke.

Four patients who experienced isolated transient global amnesia had computed tomographic evidence for a cerebral infarct (3 cases) or hemorrhage (1 case). The medial part of the temporal lobe was involved in 2 patients (left in 1, right in 1), the left lentiform nucleus in 1 patient, and the left thalamus in 1 left-handed patient. These findings suggest that transient global amnesia may be associated with stroke in some cases, but it has no localizing value within the temporodiencephalic structures. No cerebrovascular events occurred over a 1-to 5-year follow-up, suggesting that transient global amnesia with infarction or hemorrhage is not a strong predictor of further stroke.

Aged↗
PubMed1992

Isolated prolonged retrograde amnesia.

We describe a patient who had isolated retrograde amnesia of 1-year duration without anterograde amnesia after recovery from encephalitis. Single photon emission computed tomography using 123I-IMP revealed that left temporal lobe abnormality. We postulate that the learning ability for new information and recalling ability for old information involve different neural structures, and there is a possible relationship between isolated retrograde amnesia and left temporal dysfunction.

Adult↗
PubMed1988

Transient amnesia resulting from vertebral artery dissection.

Acute transient amnesia has not been previously associated with vertebral artery dissection. We describe two men with acute onset of dense anterograde amnesia and partial retrograde amnesia resulting from spontaneous vertebral artery dissection. Both amnesic syndromes completely resolved with conservative management.

Adult↗
PubMed2005

Deferred imitation of action sequences in developmental amnesia.

The aims of this study were to investigate whether patients with developmental amnesia (DA) associated with bilateral hippocampal volume reduction show an impairment in incidental nonverbal recall of action sequences, and whether the severity of this memory impairment is influenced by the sequence structure (causal vs. arbitrary). Like adult-onset cases of amnesia (McDonough, Mandler, McKee, & Squire, 1995), patients with DA did not differ significantly from their age-, sex-, and IQ-matched controls in spontaneous production of the sequences prior to modeling but recalled fewer target actions and action pairs than the control group after a 24-hour delay, independent of sequence structure. Unlike the patients with adult-onset amnesia, however, the patients with DA showed some memory for both types of sequences after a 24-hour delay. This difference in severity of memory impairment might reflect differences in extent of pathology and/or age at injury.

Adolescent↗
PubMed1997

Posttraumatic stress disorder in patients with traumatic brain injury and amnesia for the event?

Frequency of DSM-III-R posttraumatic stress disorder (PTSD) was studied in 47 active-duty service members (46 male, 1 female; mean age 27 = 7) with moderate traumatic brain injury and neurogenic amnesia for the event. Patients had attained "oriented and cooperative" recovery level. When evaluated with a modified Present State Examination and other questions at various points from study entry to 24-month follow-up, no patients met full criteria for PTSD or met criterion B (reexperience); 6 (13%) met both C (avoidance) and D (arousal) criteria. Five of these 6 also had organic mood disorder, depressed type, and/or organic anxiety disorder. Posttraumatic amnesia following moderate head injury may protect against recurring memories and the development of PTSD. Some patients with neurogenic amnesia may develop a form of PTSD without the reexperiencing symptoms.

Adult↗
PubMed1975

Amnesia following severe head injury.

This report concerns some aspects of the problem of establishing valid and reliable criteria for post-traumatic amnesia, and of relating this to other cognitive functions in the post-injury period. Of specific interest are the variability of the duration of retrograde and anterograde amnesia on attempts at repeated assessment, and the relationship between the time of return of full orientation and the end of the period of anterograde amnesia. A prospective study was undertaken of sixty consecutive patients who had suffered severe head injuries and had been admitted to the neurosurgical service of the Winnipeg General Hospital. The object of this study was to obtain information regarding organic, psychological and social indices of the future clinical course.

Amnesia↗