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A left rostral thalamic hematoma was found in a 52-year-old hypertensive man who suffered from a 10-h episode of transient global amnesia (TGA). A neuropsychological study revealed no cognitive impairment in a follow-up period for 5 years. The left rostral part of the thalamus appears to be responsible for his TGA, due probably to an interference of the mamillothalamic tract, ventroamygdalofugal pathway or dorsal noradrenergic bundle.
The possibility of naturally occurring amnesia was examined in aging Fischer F254 rats. Animals 110 weeks old showed a loss of learning and memory in a passive avoidance responses (PAR) failure test. When 120 mg/kg/day of Shosaikoto extract was placed in the diet after 72 weeks of age to 110 weeks, it improved age-induced PAR failure in both the two-compartment avoidance box test and the step-down test. The responses of 110-week-old Shosaikoto-treated rats on both PAR failures were almost the same as those of non-treated 6-week-old rats. In these Shosaikoto-treated rats, dopamine was increased and norepinephrine and vanillyl mandelic acid were decreased in brain relative to those in non-treated aging rats.
Transient global amnesia is a not uncommon presentation of acutely altered neuropsychiatric status. It is, however, a clinical diagnosis that requires a careful history with attention to inciting events, risk factors for cerebrovascular disease, the absence of other abnormalities on neurological examination, and normal results of laboratory studies. Knowledge of the generally benign course of TGA can facilitate the care and psychological support of these patients and their families.
Anterograde amnesia following triazolam ingestion lasting beyond the sedative-hypnotic effect of the drug has recently been reported. Two additional cases are presented involving emergency physicians.
We studied the effects of human recombinant interleukin-1 alpha on scopolamine-induced amnesia for a passive avoidance response in the mouse. Post-training intraperitoneal administration of the cytokine (0.25 or 0.50 microgram/mouse) significantly reduced the amnesic effect of scopolamine (1.0 mg/kg i.p.). Our results indicate that peripheral interleukin-1 alpha can influence behavior and suggest the involvement of the cholinergic system in the neuromodulatory actions of this cytokine.
We studied the effects of CGP 35348, a centrally active blocker of GABAB receptors, on scopolamine-induced amnesia for a passive avoidance response in the mouse. Both pre-training or post-training intraperitoneal administration of the GABAB antagonist (75, 150 and 300 mg/kg i.p.) significantly reduces the amnesic effect of scopolamine (1.0 mg/kg i.p.). Our results are in agreement with previous observations indicating a role for the GABAB receptors in the modulation of memory function, and suggest a possible role of GABAB receptor antagonists as nootropic drugs.
Current controversy exists regarding the role of episodic representations in the formation of long-term semantic memories. Using the drug midazolam to induce temporary amnesia we tested participants' memories for newly learned facts in a semantic cue condition or an episodic and semantic cue condition. Following midazolam administration, memory performance was superior in the episodic and semantic condition, suggesting early semantic learning is supported by episodic representations.
The cause of transient global amnesia (TGA) remains controversial. Focal cerebral ischemia, seizure, venous congestion, and migraine have all been proposed as underlying mechanisms. We describe a patient presenting with typical TGA who two days later developed a posterior circulation stroke due to basilar artery occlusion. He was treated successfully with intra-arterial thrombolytic therapy. Shortly thereafter, he had recurrent basilar artery thrombosis and jugular vein thrombosis, and was found to have a mucinous adenocarcinoma believed to be causing a hypercoagulable state. We believe this case supports the hypothesis that TGA can on occasion be caused by cerebral ischemia.
Administration of drugs activating cannabinoid CB(1) receptors in the brain induces memory deficit in rodents, and blockade of these receptors may restore memory capacity in these animals. Central administration of beta-amyloid or beta-amyloid fragments may also lead to memory disturbances. This study was undertaken to study the involvement of cannabinoid CB(1) receptors in amnesia induced by beta-amyloid fragments in mice tested in a step-through passive avoidance paradigm. Pre-training intracerebroventricular (i.c.v.) injection of beta-amyloid fragments, beta-amyloid peptide-(25-35) (4, 8 or 16 nmol/mouse) or beta-amyloid peptide-(1-42) (200, 400, 800 pmol/mouse) 7 days prior to the learning trial reduced in a dose-dependent manner the retention of passive avoidance response. This effect was observed in two retention tests, 1 and 7 days after the learning trial. The two beta-amyloid fragments showed similar potency in reducing retention of passive avoidance behavior. This effect was counteracted by a single intraperitoneal (i.p.) injection of the cannabinoid CB(1) receptor antagonist, N-(piperidin-l-yl)-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide hydrochloride (SR141716A, 1 mg/kg), made 30 min prior to the second retention test. The injection of SR141716A per se did not affect memory capacity of mice. The i.c.v. administration of beta-amyloid peptide-(25-35) (8 nmol/mouse) or of beta-amyloid peptide-(1-42) (400 pmol/mouse) made 30 min prior to the learning trial failed to affect the retention capacity of mice as measured 1 and 7 days later. Also, the i.p. injection of SR 141716A (1 mg/kg) made 30 min prior to the learning trial did not influence the behavioral response of mice injected with beta-amyloid peptide-(25-35) (8 nmol/mouse) or of beta-amyloid peptide-(1-42) (400 pmol/mouse) 7 days prior to the learning trial. These results show that beta-amyloid fragments induce a dose-dependent memory deficit. Their effect on memory retention depends upon the time of administration and seems to involve cannabinoid CB(1) receptors in the brain.
The pathogenesis and localization of neuronal dysfunction in transient global amnesia (TGA) is still disputed more than 40 years after the first description of this clinical entity. Previous studies have indicated that structural abnormality is rare in TGA. We report a case of TGA in a patient with acute ischemia in the body of right caudate nucleus. This provides evidence in support of an ischemic hypothesis as the possible etiology of TGA. The role of caudate nucleus in human memory is also reviewed.
Transient global amnesia (TGA) is a disorder of unknown aetiology, characterized by sudden loss of anterograde memory, in the absence other neurological signs or symptoms, followed by complete recovery in less than 24h. Precipitating actions such as strenuous physical activity or valsalva-like manoeuvres are frequently reported. Since first described in 1958, by Fisher and Adams, the possible pathophysiology has undergone much speculation. Nonconvulsive epileptic seizures, migraine, paradoxical embolism thorough a patent foramen ovale, and transient ischemic attacks have been proposed as potential mechanisms. One of the latest hypotheses is that venous congestion causes either ischemia or induces spreading depression in the medial temporal lobes. It has been demonstrated that retrograde flow in the internal jugular veins occurs more frequently during valsalva manoeuvres in TGA patients than in controls, supporting a dysfunctional venous circulation as part of the pathogenesis. However, earlier hypotheses typically fail to explain the relatively low recurrence rate of TGA, lack of comorbidity and the relation to precipitating events. If cerebral venous hypertension was the solely cause of TGA it would presumably be much more common with very high recurrence rates among those predisposed of the condition. Structural changes observed in MRI and SPECT studies along with reports of mild cognitive impairment lasting much longer than the amnestic episodes, indicate that TGA is less transient and perhaps somewhat less benign than earlier believed. Many cases of TGA seem to be associated with factors of increased risk of cerebral venous thrombosis, such as polycythemia, antiphospholipid antibodies, venous hypertension, female sex and more. We suggest that most cases of TGA may be due to small thrombi in the deep cerebral venous system. Small venous thrombi may difficult to visualize even when using modern imaging technology. Further studies of TGA patients with for example blood analysis of D-dimer together with MR venography or CT venography could be done to evaluate this new hypothesis.
Damage limited to the hippocampus is believed to result in temporally graded retrograde amnesia (RA), with more severe RA occurring only as a result of additional damage to adjacent neocortical structures. Patient N.T. suffered dense, temporally ungraded, RA following a right temporal lobectomy for intractable epilepsy. Postmortem pathological examination revealed sclerosis of the unresected left hippocampus. Microscopic analysis of the parahippocampal areas and other temporal lobe regions undertaken in this study confirmed the absence of any significant pathology extending beyond the hippocampus. This further review of the pathological findings in N.T. is therefore not consistent with the postulated role of the hippocampus as a temporary memory store and suggests instead that the hippocampus is involved in the storage of remote memories as well as recent memories.
This is the introduction of Drosophila into the study of learning and memory affected by removal of the geomagnetic field (GMF) for successive generations. Using the operant visual learning/memory paradigm at a flight simulator, the present study revealed that wild-type flies raised in a hypomagnetic field environment continuously for 10 successive generations were gradually impaired in visual conditioning learning and memory formation and finally the 10th generation flies became morphs of nonlearners and completely amnesiac. The control experiments show that the impairment could not be ascribed to any apparent sensorimotor problems in Drosophila. The reverse shift from hypomagnetic field (HMF) to natural GMF restored the GMF-free induced amnesia fully after six consecutive generations. Thus, our findings demonstrate conclusively that some serious, but reversible learning and memory impairment may occur for living organisms in a prolonged separation from GMF over many consecutive generations. And Drosophila has the potential to develop into a new model organism for the study of the neurobiology of magnetism for multiple generations.
Baddeley and Wilson [Baddeley, A. D., & Wilson, F. B. (2002). Prose recall and amnesia: implications for the structure of working memory. Neuropsychologia 40, 1737-1743.] have argued that their finding of a positive association between amnesics' immediate prose recall scores and their scores on measures of executive function and fluid intelligence supports the view that an episodic buffer exists. However, the pattern of data from amnesics tested in our laboratory presented some problems for this conceptualisation of the episodic buffer.
The present study examined remote spatial memory in a test that spans several months to determine whether remote memories are spared relative to more recent ones, as predicted by models of memory consolidation. At 3, 6 or 12 months of age, groups of rats received forced-choice training as to the location of food reward in a cross maze. At 12.5 months, rats received bilateral neurotoxic lesions to the hippocampus or a control surgical procedure and 2 weeks later their memory for the spatial location was tested. Their performance was compared to that of rats with hippocampal or control lesions with no prior training on several measures of savings. The hippocampal group with no pre-training, as expected, was severely impaired in learning the location of the food reward. Compared to this group, rats with hippocampal lesions that were pre-trained consistently performed better at the shortest training-surgery interval but not at the longer ones. That is, rats with hippocampal lesions exhibited retrograde amnesia at all training-surgery intervals and a forgetting curve that paralleled that of the control groups. The results were interpreted within a framework that distinguishes between relational and associative context, and as providing evidence that the hippocampus is necessary for the retention and retrieval of memories that are bound to relational context, regardless of the age of the memory.
Functional brain imaging studies of priming assume that the behavioral facilitation and activity reductions resulting from multiple repetitions reflect the continued tuning of processes engaged during the initial processing of items. Utilizing an object priming paradigm in which participants were asked to make relative size judgments about visually presented common objects, we tested an alternate hypothesis that states that with multiple repetitions participants come to rely on a more efficient response learning mechanism. In experiment 1, the decision cue was inverted such that previous judgments made either once or three times were rendered invalid. Decision inversion resulted in a reduction of all priming, but most critically, led to a reduction of multiple-repetition priming to the level of single-repetition priming. In experiment 2, patients with amnesia failed to show a priming advantage for multiple repetitions, indicating that response learning is dependent on the medial temporal lobes. Taken together, these results suggest that a different process increasingly mediates priming behavior as repetitions increase. With repeated exposure, behavioral facilitation rapidly comes to reflect a more efficient response learning mechanism rather than facilitated access to object knowledge.
ED, a 83-year-old woman, meets the criteria of pure progressive amnesia, with gradual impairment of episodic and autobiographical memory, sparing of semantic processing and strong working memory (WM) deficit. The dissociation between disturbed WM and spared semantic processing permitted testing the role of WM in processing anaphors like pronouns or repeated names. Results showed a globally normal anaphoric behavior in two experiments requiring anaphoric processing in sentence production and comprehension. We suggest that preserved semantic processing in ED would have compensated for working memory deficit in anaphoric processing.
Previous work has reported that in the Iowa gambling task (IGT) advantageous decisions may be taken before the advantageous strategy is known [Bechara, A., Damasio, H., Tranel, D., & Damasio, A. R. (1997). Deciding advantageously before knowing the advantageous strategy. Science, 275, 1293-1295]. In order to test whether explicit memory is essential for the acquisition of a behavioural preference for advantageous choices, we measured behavioural performance and skin conductance responses (SCRs) in five patients with dense amnesia following damage to the basal forebrain and orbitofrontal cortex, six amnesic patients with damage to the medial temporal lobe or the diencephalon, and eight control subjects performing the IGT. Across 100 trials healthy participants acquired a preference for advantageous choices and generated large SCRs to high levels of punishment. In addition, their anticipatory SCRs to disadvantageous choices were larger than to advantageous choices. However, this dissociation occurred much later than the behavioural preference for advantageous alternatives. In contrast, though exhibiting discriminatory autonomic SCRs to different levels of punishment, 9 of 11 amnesic patients performed at chance and did not show differential anticipatory SCRs to advantageous and disadvantageous choices. Further, the magnitude of anticipatory SCRs did not correlate with behavioural performance. These results suggest that the acquisition of a behavioural preference--be it for advantageous or disadvantageous choices--depends on the memory of previous reinforcements encountered in the task, a capacity requiring intact explicit memory.