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PubMed1998

Cerebral perfusion during transient global amnesia: findings with HMPAO SPECT.

UNLABELLED: The aim of this study was to investigate the pattern of regional cerebral blood flow changes associated with transient global amnesia (TGA). METHODS: HMPAO SPECT was performed in six consecutive patients during the acute phase of TGA. A follow-up SPECT was performed 3-20 wk later in four of the six patients. Semiquantitative analysis of 14 regions of interest, including the basal ganglia and the basal section of the temporal lobes, was performed by comparing patient data with control data obtained from a matched group of healthy subjects. RESULTS: During TGA, unilateral or bilateral hypoperfusion of the temporo-basal region was observed in four patients. Variable hypoperfusion of further cortical areas was observed in five patients. Two patients who exhibited the most marked cortical hypoperfusion also showed striatal and thalamic hypoperfusion. These changes were normalized in the control studies obtained in four patients. CONCLUSION: It remains unclear whether hypoperfusion during TGA represents a primary feature or a sequel of regional brain hypometabolism. Because hypoperfusion is not confined to the temporo-basal region or to the territory of the posterior cerebral artery, it is suggested that the origin of TGA-related changes lies at the level of subcortical structures that project diffusely to the cerebral cortex.

Acute Disease↗
PubMedDate not supplied

Transient global amnesia.

Transient global amnesia is an alarming but benign disorder of middle age, which prevents both the formation of new memories, and the retrieval of recently formed ones, for some hours. Research over the last 10 years has shed light on the epidemiology, neuropsychology, functional anatomy and differential diagnosis of this distinctive condition, and clarified its management.

Adult↗
PubMed1998

Ipidacrine (NIK-247), a novel antidementia, rapidly enters the brain and improves scopolamine-induced amnesia in rats during the Morris water maze task.

The effects of single and repeated administrations of ipidacrine (NIK-247, 9-amino-2, 3, 5, 6, 7, 8-hexahydro-1H-cyclopenta [b] quinoline monohydrochloride monohydrate) on scopolamine-induced spatial learning deficit were investigated in rats using the Morris water maze task. A single oral administration of ipidacrine (0.3 and 1 mg/kg) reduced the increased total latency induced by scopolamine in this task. The repeated administration of ipidacrine (1 mg/kg) of once a day for 5 successive days reduced the increased total latency induced by scopolamine to the levels of the saline-treated control rats in this task. In this pharmaco-kinetic study, ipidacrine was rapidly taken up into the brain within 5 min. Moreover, higher drug levels were observed mainly in the cortex and hippocampus, which both play important roles in learning and memory. Thus, a previous study together with this investigation indicate that ipidacrine improves amnesia which consists of the impairment of the working and reference memory in various animal models, suggesting that ipidacrine is a useful candidate for the therapy of patients with Alzheimer's disease.

Aminoquinolines↗
PubMed1998

Resting and acetazolamide-challenged technetium-99m-ECD SPECT in transient global amnesia.

Regional resting cerebral blood flow and vascular reserve in a patient with transient global amnesia (TGA) were evaluated during and after a TGA episode using 99mTc-ethyl cysteinate dimer (ECD). The patient had consecutive SPECT studies before and after acetazolamide (ACZ) administration with adjunctive radionuclide angiography using equal-volume-split 99mTc-ECD. SPECT study during TGA episode showed poor vasodilatory reactivity to ACZ in the left medial temporal region involving the hippocampus and resting hypoperfusion in the regions bilaterally. The resting hypoperfusion with reserved vasodilatory reactivity to ACZ also was seen in the bilateral thalami. Abnormal findings in these regions disappeared on the follow-up SPECT study 15 days after the onset. No previous SPECT evaluation of regional abnormalities of both hemodynamic reserve and resting perfusion during and after an episode of TGA has been reported.

Acetazolamide↗
PubMed1999

Temporally graded retrograde amnesia of contextual fear after hippocampal damage in rats: within-subjects examination.

We have shown previously that electrolytic lesions of the dorsal hippocampus (DH) produce a severe deficit in contextual fear if made 1 d, but not 28 d, after fear conditioning (). As such, the hippocampus seems to play a time-limited role in the consolidation of contextual fear conditioning. Here, we examine retrograde amnesia of contextual fear produced by DH lesions in a within-subjects design. Unlike our previous reports, rats had both a remote and recent memory at the time of the lesion. Rats were given 10 tone-shock pairings in one context (remote memory) and 10 tone-shock pairings in a distinct context (with a different tone) 50 d later (recent memory), followed by DH or sham lesions 1 d later. Relative to controls, DH-lesioned rats exhibited no deficit in remote contextual fear, but recent contextual fear memory was severely impaired. They also did not exhibit deficits in tone freezing. This highly specific deficit in recent contextual memory demonstrated in a within-subjects design favors mnemonic over performance accounts of hippocampal involvement in fear. These findings also provide further support for a time-limited role of the hippocampus in memory storage.

Acoustic Stimulation↗
PubMed1997

Thalamic amnesia following venous infarction: evidence from a single case study.

The present paper describes the case of a right-handed Italian-English bilingual male patient suffering from amnesia following a bilateral thalamic lesion due to venous infarction. Within a few months from the onset, the lesion gradually shrank and was finally confined to the left thalamus only, in particular to the antero-medial portion and the pulvinar. The mammillary bodies and the cortical areas of both hemispheres were spared. After the regression of a series of generalized cognitive deficits implying slow psychic activity confusion, and spatial and temporal disorientation, the patient presented a persistent amnesic syndrome with mild language disorders, both in Italian and in English. Major disorders of memory included a dissociation between verbal memory, which was severely impaired, and spatial memory, which was largely preserved.

Brain Ischemia↗
PubMed1995

Steps toward healing: false memories and traumagenic amnesia may coexist in vulnerable populations.

Child abuse is surely the most agonizing psychological issue of our time. We decry the tendency to polarize around the either-or dichotomy of "recovered versus false memories," when both are likely to occur. Memory researchers seem to generalize from the mild, one-shot stressors of the laboratory to the severe repeated traumas reported by abused populations, an inferential leap that is scientifically dubious. Naturalistic studies show (a) some post-traumatic memory impairment (not just forgetting, but difficulty remembering in spite of repeated efforts); (b) dissociativity, such as emotional numbing, detachment, and the like; but also (c) increased suggestibility (Spiegel & Cardena, 1991). About 20% of the normal population is highly suggestible, and in these individuals it is trivially easy to show suggested amnesia, detachment, perceptual blocking, etc., as well as to suggest dramatically false memories. It is therefore vital to assess suggestibility and dissociativity in traumatized populations. Adult survivors of abuse may show both more false "memories" and more "false forgetting" than the normal population.

Adolescent↗
PubMed1995

What infant memory tells us about infantile amnesia: long-term recall and deferred imitation.

Long-term recall memory was assessed using a nonverbal method requiring subjects to reenact a past event from memory (deferred imitation). A large sample of infants (N = 192), evenly divided between 14- and 16-months old, was tested across two experiments. A delay of 2 months was used in Experiment 1 and a delay of 4 months in Experiment 2. In both experiments two treatment groups were used. In one treatment group, motor practice (immediate imitation) was allowed before the delay was imposed; in the other group, subjects were prevented from motor practice before the delay. Age-matched control groups were used to assess the spontaneous production of the target acts in the absence of exposure to the model in both experiments. The results demonstrated significant deferred imitation for both treatment groups at both delay intervals, and moreover showed that infants retained and imitated multiple acts. These findings suggest that infants have a nonverbal declarative memory system that supports the recall of past events across long-term delays. The implications of these findings for the multiple memory system debate in cognitive science and neuroscience and for theories of infantile amnesia are considered.

Attention↗
PubMed1995

Episodic memory and autonoetic consciousness: developmental evidence and a theory of childhood amnesia.

This research draws together Tulving's (1985) view on episodic memory and research on children's developing "theory of mind." Episodic memory, in its technical meaning given by Tulving, requires the autonoetic consciousness of having experienced remembered events, but developmental findings suggest that children cannot encode events as experienced before the age of about 4 or 5 years. Before this age they have insufficient understanding of what constitutes experience, specifically they do not reflect on the perceptual origin of their own knowledge. To demonstrate such a link children between 3 and 6 years were assessed for their understanding of the perceptual origin of their own knowledge on different "see-know tests," in particular a test assessing understanding that our senses inform only about certain aspects of the perceived objects. A significant association was found between passing see-know tests and free recall, which persisted even when cued recall and verbal intelligence are partialed out. These results are used to argue that between 3 to 6 years children develop the ability to remember events as experienced and that this development can explain adults' inability to have recollective experiences of childhood events before that age (childhood amnesia).

Association Learning↗
PubMed1999

Stimulators of the cAMP cascade reverse amnesia induced by intra-amygdala but not intrahippocampal KN-62 administration.

Infusion of the calcium-calmodulin-dependent protein kinase II (CaMKII) inhibitor KN-62 (3.5 ng/side) 0 h after training into rat hippocampus CA1 or amygdala has been known for years to cause retrograde amnesia for step-down inhibitory avoidance. On the other hand, drugs that indirectly stimulate protein kinase A (PKA) (8-Br-cAMP, 1.25 microg/side; norepinephrine, 0.3 microg/side; the dopamine D1 receptor agonist, SKF38393, 7.5 microg/side) infused 3 h posttraining into CA1 but not amygdala markedly facilitate retention of this task. Here we find that 8-Br-cAMP, norepinephrine, or SKF38393 given 3 h posttraining into rat CA1 reverses the amnestic effect of KN-62 given into the amygdala 0 h after training, but not that of KN-62 given into CA1 0 h posttraining. The findings bear on the participation of CaMKII and of the cAMP/PKA cascade in memory processes in the hippocampus and the amygdala. Both cascades have been proposed to play a role in memory: CaMKII in the early phase and PKA in the transition between the early phase and long-term memory. Clearly, in CA1, both cascades are involved and are crucial, and the CaMKII cascade must precede the PKA cascade. In contrast, in the amygdala, only the CaMKII cascade is active, and it does not play a central role in memory, inasmuch as its deleterious effect may be fully recovered by stimulation of the PKA cascade in the hippocampus. This further supports the contention that the hippocampus is essential for memory formation of this task, as it is for many others, whereas the amygdala appears to play instead an early modulatory role.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1999

Chloramphenicol-induced amnesia for passive avoidance training in the day-old chick.

The antibiotic chloramphenicol, an inhibitor of mitochondrial protein synthesis, was used to investigate the time-related changes in protein synthesis following passive avoidance training in the day-old chick (white leghorn-black Australorp). Retention of memory for this simple learning task is known to be prevented by an inhibitor of cytosolic protein synthesis, anisomycin, in a biphasic manner, with the first phase of sensitivity occurring up to 90 min post-training and the second phase between 4 and 5 h post-training (Freeman, Rose, & Scholey, 1995). Birds received bilateral intracranial injections of chloramphenicol (10 microl/hemisphere of a 7.4 mM solution) at various times relative to training and were tested 24 h later. This report shows that at the second phase of anisomycin susceptibility there was a chloramphenicol-sensitive period (5 h post-training) which had an onset time less than 1 h after injection. The effect of chloramphenicol appears not to be due to the mitochondria being energetically compromised since intracranial injections of an uncoupler of mitochondrial oxidative phosphorylation, 2,4-dinitrophenol (0.1 mM), did not disrupt memory formation when injected 5 h after training, even though it did cause amnesia when injected at the earlier time point of 20 min post-training. These results are discussed in the context of what is already known about memory formation in the day-old chick.

Animals↗
PubMed1979

DDC-induced amnesia and norepinephrine: a correlated behavioral-biochemical analysis.

Diethyldithiocarbamic acid (DDC), a dopamine-B-hydroxylase inhibitor, when injected into rats 30 min to 6 h before training of a passive avoidance task, impaired formation of long-term memory as indicated by performance on a retention test 24 h later. Performance of the task was at its minimum when injection occurred 2 to 4 h prior to training; recovery was evident in animals trained 5 or 6 h after drug treatment. Catecholamine assay of brains of temporally yoked animals showed that norepinephrine depletion followed a time course paralleling that of the amnesia. These findings support the hypothesis that the degree of memory storage, as reflected in performance following training in a passive avoidance task, can be directly correlated with the level of norepinephrine existing at the time of training.

Animals↗
PubMed1995

Persistent pure verbal amnesia and transient aphasia after left thalamic infarction.

A 57-year-old right-handed man suffered persistent pure verbal amnesia (PPVA) and transient aphasia after left thalamic infarction. A neuroanatomical study with magnetic resonance imaging to identify the site of the lesion showed destruction of the internal medullary lamina (IML), mammillothalamic tract (MTT), the ventrolateral nucleus (VL) and the lower one-third of the medial nucleus. As regions critical for PPVA are unknown, we reviewed the cases of PPVA after left thalamic infarction reported in the literature. These suggest that confined destruction of the IML, MTT and VL in the left thalamus can produce PPVA.

Anomia↗
PubMed1988

Time courses of amnesia development in two areas of the chick forebrain.

The roles of different forebrain structures in stages of memory formation were investigated by injecting agents into either the left medial hyperstriatum ventrale (MHV) or right lateral neostriatum (LNS) close to the time of one-trial taste-avoidance training. With L-glutamate injected into either the left MHV or right LNS 5 minutes pretraining, retention was good 1 minute posttraining but significantly impaired at 5 minutes and each subsequent time point. With emetine injected into either area, retention was still good 60 minutes posttraining but significantly impaired at 90 minutes. With ouabain, retention declined more slowly following injection into the right LNS (at 45 minutes) compared to injection in the left MHV (at 30 minutes). A second experiment confirmed the regional difference in amnesia development produced by ouabain. These results indicate that the duration of short-term memory is longer following inhibition of intermediate-term memory (ITM) in the right LNS, compared to inhibition of ITM in the left MHV.

Animals↗
PubMed1990

Central muscarinic activities of an M1-selective agonist: preferential effect on reversal of amnesia.

Effects of FKS-508 (AF102B; cis-2-methylspiro (1,3-oxathiolane-5,3')-quinuclidine), a novel M1-selective agonist, on central muscarinic responses in mice were examined in comparison with oxotremorine. FKS-508 was slightly less potent (6 times) in reversal of scopolamine-induced amnesia (passive avoidance failure), but far less potent (260 and 55 times) in producing hypothermia and tremor than oxotremorine. These results show that the selective M1 agonist FKS-508 differentiates highly between the central muscarinic effects.

Animals↗
PubMed1985

The perceptual priming phenomenon in amnesia.

Alcoholic Korsakoff patients and controls were given three variants of a priming task. In the first task, a study list of words was followed by a recognition test phase and then a perceptual identification test phase. In the second task, the order of the two test phases was reversed. The amnesics performed like normals on the priming for identification task and the delay did not affect their performance. However, recognition by amnesics was significantly impaired when the delay was introduced; although it too was normal with no delay. In a third task, pseudowords were used as stimuli. Under these conditions the amnesics could not be primed nor could they recognize the material. The implications of these findings for current theories of amnesia were discussed.

Alcohol Amnestic Disorder↗
PubMed1988

The performance of amnesic subjects on tests of experimental amnesia in animals: delayed matching-to-sample and concurrent learning.

A group of amnesic Korsakoff subjects and a group of alcoholic controls were trained on a test of visual recognition, delayed matching-to-sample with trial unique stimuli. This test was modelled on comparable tasks used in the development of animal models of human amnesia. It was found that the Korsakoff subjects were severely impaired when the task difficulty was increased by lengthening the retention delay beyond 10 sec or by increasing the number of items intervening between sample presentation and test. The amnesic subjects were also impaired on the acquisition of a set of concurrent visual discriminations. These results bear clear similarities to those obtained from experimental amnesic syndromes in monkeys.

Adult↗
PubMed1989

Amnesia and memory for modality information.

In this study, lists of words were used in a mixed-modality fashion (some read aloud by the subject, others read only by the experimenter). They were presented in this format to both Korsakoff amnesics and matched controls, with subjects only told to remember the words themselves. Controls and amnesics were matched on item-memory (forced-choice recognition) by using longer lists, tested at longer delays, for the controls. Despite this, however, the controls performed significantly better than the amnesics at modality-identification judgements about the items chosen during recognition. Whether the reported result reflects the memory deficit which causes amnesia, or whether it is more properly attributed to additional (frontal lobe) pathology present in only certain amnesics, is discussed.

Adult↗