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Transient global amnesia associated with a single metastasis in the non-dominant hemisphere. Case report.

A patient in whom transient global amnesia (TGA) led to the diagnosis of a metastasis of a transition-cell carcinoma of the bladder to the non-dominant hemisphere is described. In previously reported cases of TGA associated with brain tumors, the tumors involved either the dominant or both hemispheres. The etiology of TGA associated with a brain tumor is most likely vascular, as suggested by the sudden development and the transitory character of the event. In contrast to the "common" form of TGA (where both temporal lobes suffer temporary ischemia), in these patients only one side of the limbic system is affected, because a brain tumor has already compromised the other limbic area. Therefore, the dominance of the hemisphere with the tumor is of no consequence, as both hemispheres have been involved. It is concluded that the TGA in these patients is not due to, but is rather associated with, a unilateral brain tumor.

Aged↗

Amnesia syndrome following left anterior thalamic infarction; with intrahemispheric and crossed cerebro-cerebellar diaschisis on brain SPECT.

We report a 61-year-old right-handed man developing disturbance of memory after a discrete thalamic infarction. Neuropsychological assessment revealed deficits in memory with retrograde and anterograde components, especially for verbal material. Brain MRI showed a left anterior thalamic infarction with normal angiographic findings. Despite the small lesion in the thalamus, he showed prolonged memory disturbance and a Brain SPECT image revealed decreased uptake in the ipsilateral fronto-temporo-parietal cortex and contralateral cerebellum. This diaschisis, a phenomenon caused by disconnection of the neural pathway helped us to evaluate the functional state of the patient and this imaging technique was valuable for obtaining to get more information for the evaluation of the neurological state and neuronal connections. In conclusion our findings correspond well with the understanding of amnesia as a disconnection syndrome because of the evidence of diaschisis on the Brain SPECT image.

Amnesia↗

Fragment memories mark the end of childhood amnesia.

Adults described and dated two kinds of first remembrances: a personal event memory (the recollection of a personal episode that had occurred at some time in some place) and a memory fragment (an isolated memory moment having no event context and remembered, perhaps, as an image, a behavior, or an emotion). First fragment memories were judged to have originated substantially earlier in life than first event memories--approximately 3 1/3 years of age for first fragment memories versus roughly 4 years of age for first event memories. We conclude that the end of childhood amnesia is marked not by our earliest episodic memories, but by the earliest remembered fragments of childhood experiences.

Adult↗

Consolidation theory and retrograde amnesia in humans.

Recent research on the cognitive dysfunctions experienced by human anmesic patients indicates that very long term (multidecade) changes may occur in memory. Flat retrograde amnesia (RA), consisting of a uniform memory deficit for information from all preamnesia time periods, indicates a simple, monolithic retrieval problem, whereas graded RA, with greater memory deficits for information from recent as opposed to remote time periods, suggests the presence of a gradual long-term encoding, or consolidation, process. An evaluation of 247 outcomes from 61 articles provides strong evidence of graded RA across different cerebral injuries, materials, and test procedures, as well as in measures of both absolute and relative (patient vs. control) performance. Future conceptualizations of human memory should address the possibility that memories increase in resistance to forgetting, or reduction in trace fragility, across many decades.

Adult↗

Is categorization performance really intact in amnesia? A meta-analysis.

Most published studies of category learning in amnesia have reported intact categorization performance. These results have been used to challenge single-system accounts of categorization and recognition, in which a single representational system mediates performance in these two tasks. Many of the published studies, however, have shown a numerical advantage for controls over amnesics and often have had low statistical power. A meta-analysis was conducted to assess whether this numerical advantage is significant when the data are pooled across studies. This analysis indicates that amnesic subjects do, in fact, show deficits in categorization tasks, which is consistent with single-system exemplar model predictions.

Amnesia↗

Nonverbal priming in amnesia.

In this experiment, we examined whether a group of well-characterized amnesic patients would exhibit normal priming for novel nonverbal materials after a single exposure. Both amnesic patients and normal control subjects studied line figures and were then given a priming test in which they were asked to reproduce both old (studied) and new (unstudied) figures after a brief exposure. The measure of priming was the number of old patterns drawn correctly relative to the number of new patterns drawn correctly. Both subject groups reproduced more old patterns than new patterns, and the effect was similar in the two groups. In contrast, amnesic patients were significantly impaired on a recognition memory test for the items that had been presented. This study contributes to recent evidence that implicit memory can support the rapid acquisition of novel verbal and nonverbal information. Perceptual priming for such material is independent of the structures damaged in amnesia.

Aged↗

Normal McCollough effect in Alzheimer's disease and global amnesia.

The McCollough effect (ME), a long-lasting, pattern-contingent aftereffect in normal human vision, was examined in persons with known deficits in memory. We induced MEs in 11 subjects, 5 patients with various severities of Alzheimer's disease (AD), H.M. (a patient who has global amnesia due to bilateral medial temporal lobectomy and who has been studied for 35 years since his operation), and 5 control subjects. H.M. and the AD patients showed MEs of strength and duration comparable to those of the control subjects. These results demonstrate a dissociation between learning mechanisms that mediate recall and recognition versus mechanisms that mediate the ME. Furthermore, knowledge about the sites of neuropathology in H.M. and in AD are consistent with other sources of evidence implicating early visual areas, especially V1, as a critical locus of the ME.

Aged↗

Focal retrograde amnesia and the episodic-semantic distinction.

This article reports a review of focal retrograde amnesia (FRA), or the phenomenon of organically based severe memory loss restricted to retrograde, or pretraumatic, memory. Cases of FRA are classified according to the type of memory loss: episodic, semantic, or both. A few different clusters of the disorder were identified. Lesions to either the anterior temporal lobes or the posterior/visual cortex can result in an FRA that devastates retrograde episodic memory, while having smaller effects on semantic memory. A number of left-hemisphere patients have FRA confined to semantic memory. There are several additional examples of FRA following minor cerebral trauma that disrupts either episodic memory alone or both episodic and semantic memory that are not accompanied by evidence of structural brain lesions. We discuss these different profiles of FRA and their implications for the understanding of memory retrieval.

Amnesia, Retrograde↗

The role of explicit memory processes in cross-modal priming: an investigation of stem completion priming in amnesia.

To clarify the role of explicit memory processes in cross-modal priming, two experiments examined the status of cross-modal stem completion priming in amnesia. Experiment 1 used a standard behavioral paradigm in which stems corresponding to studied and unstudied words were intermixed. Amnesic patients showed intact within- and cross-modal priming, but, in contrast to controls, they recognized very few of their completions as having been on the study list. This finding suggests that memorial awareness is not necessary for cross-modal priming to occur. Experiment 2 used a paradigm modeled after functional imaging studies, in which stems corresponding to studied and unstudied words were blocked. Amnesic patients showed intact within-modal priming, but impaired cross-modal priming. This finding is consistent with the notion that a blocked format induces voluntary retrieval strategies in normal participants.

Amnesia, Anterograde↗

Disproportionate deficit in associative recognition relative to item recognition in global amnesia.

In two experiments, we tested the hypothesis that medial temporal lobe (MTL) amnesic patients and, likewise, diencephalic (DNC) amnesic patients evidence a disproportionate deficit in memory for associations in comparison with memory for single items. In Experiment 1, we equated item recognition in amnesic and control participants and found that, under these conditions, associative recognition remained impaired both for MTL patients and for DNC patients. To rule out an alternative interpretation of the results of Experiment 1, in Experiment 2 we compared the performance of amnesic and control participants on a one-item recognition task and a two-item recognition task that required no memory for the association between members of word pairs. In the MTL group, when single-item recognition was equated to that of the controls, two-item nonassociative pair memory was equivalent as well. In the DNC group, nonassociative pair memory was impaired, but this impairment did not fully account for the impairment in associative memory. These findings indicate that memory for novel associations between items is disproportionately impaired in comparison with memory for single items in amnesia.

Adult↗

[Transient global amnesia].

Transient global amnesia is a disease of nonuniform pathogenesis. Based on review of the literature, etiology, prevalence, clinical pictures and differentiation of this interesting but not always recognized syndrome have been discussed in the article.

Amnesia↗

Interaction between midazolam-induced anterograde amnesia and memory enhancement by treatments given hours later in hippocampus, entorrhinal cortex or posterior parietal cortex.

Rats were bilaterally implanted with indwelling cannulae in the CA1 region of the dorsal hippocampus, the entorrhinal cortex or the posterior parietal cortex. After recovery from surgery, they were trained in a one-trial step-down inhibitory avoidance task using a 0.3 mA footshock. The animals received i.p. 15 min before training either saline (1 ml/kg) or midazolam (1 mg/kg). Three hours after training they received, through the cannulae, infusions of saline, norepinephrine (0.3 microg/side), SKF38393 (7.5 microg/side), or 8-Br-cAMP (1.25 microg/side) into the brain regions mentioned. Animals were tested for retention 24 h after the training session. Midazolam produced anterograde amnesia, and the post-training treatments (with the exception of SKF38393 given into the entorrhinal cortex) caused retrograde memory facilitation. The amnestic effect of midazolam and the facilitatory effect of the treatments given into the brain cancelled each other out. Therefore, the mechanisms triggered by midazolam can interact with others in areas involved in memory processing several hours after their onset.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

[Is "scopolamine-induced amnesia" in rats the result of state-dependent learning?].

The effects of a single and repetitive administration of m-cholinoblocker scopolamine (Sc) to male rats on retention of step-through passive avoidance (PA) or active avoidance (AA) in a shuttle-box were compared. In case of PA Sc (1 mg/kg) was injected i.p. only 30 min before training, only 30 min before testing, or both before training and before testing. In case of AA Sc (0.5 mg/kg/day) was injected i.p. only 15 min before each training session or both before training and before testing (44 days after achievement of learning criterion). The PA and AA retention were impaired only in the experiments, where the drug was administered before training, but did not differ from control, when Sc was injected twice. The Sc-induced amnesia (like many other cases of memory deficits) is suggested to be a manifestation of state-dependent learning. Similarity between the brain state during memory consolidation and during the retention test is necessary for recollection.

Acoustic Stimulation↗

[Transient global amnesia: a review of 58 cases].

INTRODUCTION: Transient global amnesia (TGA) is a clinical condition in which the etiopathogenesis is still not clear. The most generally accepted theory is of a vascular origin, although epilepsy or migraine have also been considered to possibly be the cause. OBJECTIVE: To make a retrospective review of the risk factors, etiopathogenesis and clinical characteristics of 58 patients with TGA. PATIENTS AND METHODS: The variables recorded were compared with those from two control groups: one of healthy individuals and one of patients with transient ischemic attacks (TIA). RESULTS: The average age of the patients with TGA was 66.01 years. The risk factors included: arterial hypertension (58.62%), dyslipemia (15.51%) and migraine (8.62%). In three patients the EEG showed weak bilateral frontotemporal interference. Cerebral CT scans were done in all cases and were found to be pathological in 23, with lacunar multinfarct the commonest abnormality. With regard to patients with TIA, these were older (66.01 vs 72.94), smoked more (1.72% vs 12.06%) and a previous stroke was more frequent (8.62% vs 31.03%). We did not find differences regarding dyslipemia, atrial fibrillation, arterial hypertension or cardiac ischemia. However, the prevalence of vascular risk factors was significantly higher in patients with TGA as compared to healthy controls. CONCLUSION: We suggest that the etiopathogenesis of TGA is probably a transient ischemic phenomenon triggered (or not) following an attack of migraine.

Adult↗

Retrograde amnesia for spatial memory induced by NMDA receptor-mediated long-term potentiation.

If information is stored as distributed patterns of synaptic weights in the hippocampal formation, retention should be vulnerable to electrically induced long-term potentiation (LTP) of hippocampal synapses after learning. This prediction was tested by training animals in a spatial water maze task and then delivering bursts of high-frequency (HF) or control stimulation to the perforant path in the angular bundle. High-frequency stimulation induced LTP in the dentate gyrus and probably also at other hippocampal termination sites. Retention in a later probe test was disrupted. When the competitive NMDA receptor antagonist 3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid (CPP) was administered before the high-frequency stimulation, water maze retention was unimpaired. CPP administration blocked the induction of LTP. Thus, high-frequency stimulation of hippocampal afferents disrupts memory retention only when it induces a change in the spatial pattern of synaptic weights. The NMDA receptor dependency of this retrograde amnesia is consistent with the synaptic plasticity and memory hypothesis.

Afferent Pathways↗

[Post-traumatic amnesia syndrome].

INTRODUCTION: Mnesic deficits are frequent in subjects which have suffered from head injury and may persist during may years. OBJECTIVE: We will analyze posttraumatic amnesia characteristics (PTA) as well as learning and memory deficits which are normally observed once the PTA phase is over. DEVELOPMENT: The PTA is defined as the period that follows a brain injury in which the affected person is incapable of consistently remembering at least the last 24 hours. That is, the period after the head injury in which the incorporation of new information in long term memory is not possible. The study of PTA has generally been focussed on the analysis of the alterations of temporo-spatial orientation and mnesic deficits, however other cognitive and behavioral alterations do exist (linguistic, attentional, critical judgement, information processing, perception, etc.), and they are associated with the particular memory disorder that we are studying, given their influence on it. We will take on board the different theories that have been proposed to explain mnesic deficits which occur during the PTA phase: lack of consolidation of new information within longterm memory; recall deficit as a result of inefficient coding of information; failures of the mechanisms to carry out the process of consolidation-recall, and poor organization in the coding of new material. We will put forward a guide for the neuropsychological assessment of memory based on the analytic and concrete study of each mnesic cognitive component, sustained generally by specific neurophysiological functional systems which allow us to establish a diagnosis, prognosis, and adequate therapeutic focus for each concrete case.

Amnesia↗

[Neurophysiological characteristics of transitory global amnesia syndrome].

Twenty seven patients with transitory global amnesia (TGA) in acute and remote (after 7 and more days) stages and 31 dyscircular encephalopathy patients with subjective memory disturbances (control group) have been examined. According to electroencephalographical (EEG) data and wave P300 cognitive evoked potential evaluation, the differences in the beta 1-activity between these groups have been found. beta 1-Activity expression on EEG correlated in different ways with latent P300 periods, increasing together with latent period (r = 0.43) in control group and decreasing in TGA (r = -0.23). The most distinct, changes were expressed in central cerebral regions. The authors hold that the relationship between changes of EEG and cognitive evoked potential in acute and remote TGA stages, as well as in control group, indicate functional character of TGA syndrome, being unrelated to cerebral structure damage.

Aged↗

[A lesion diagnosed by MRI in a case of transient global amnesia].

Transient global amnesia(TGA) had been recognized as a disease without abnormal findings on neuroimaging before magnetic resonance(MRI) imaging was practicable. Recently, abnormal findings on MRI reported in cases of TGA. We here reported a case of TGA showing a transient abnormal intensity in left hippocampus on MRI diffusion-weighted image. A 52-year-old man suddenly became to unable to keep his recent memory without histories of trauma or epilepsy. He showed no abnormal neurologic findings excepting for the recent memory. MRI performed within an hour after onset demonstrated no abnormality on T1- and T2-weighted images. Diffusion-weighted image (b = 1,000) showed hyperintensity in the left medial temporal lobe, and the apparent diffusion coefficient(ADC) in this region was lower(72.8 cm2/s) than that in the contralateral region(94.4 cm2/s). TGA was completely resolved 17 hours after onset.

Amnesia↗