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Query: UMLS:C0002622 (amnesia)
 5,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The case of an alcoholic man is reported who survived a suicidal hanging attempt, and subsequently suffered of amnesia, dementia, apathy and behavioural abnormalities. A clinical diagnosis of hypoxic brain damage was made, but upon autopsy six years later, extensive pseudosystematic thalamic degeneration and mammillary body atrophy were found, indicating a status post Wernicke encephalopathy. Precipitation of the disease is attributed to the synergetic effect of cerebral hypoxia/ischemia and thiamine deficiency.
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PMID:Wernicke-Korsakoff syndrome following attempted hanging. 823 15

The effects of opioid peptides selective for opioid receptors on drinking, dopamine-related behavior, discriminative stimulus and memory processes were investigated in detail. Mu opioid receptors in the paraventricular nucleus of hypothalamus played an important role in drinking behavior. The stimulation of mu and kappa opioid receptors inhibited dopamine D2 receptor-related behavior. The discriminative stimulus effects of morphine and pentazocine were mediated through mu opioid receptors, while the stimulus effects of cocaine through delta opioid receptors. Mu opioid agonists elicited memory dysfunctions, whereas kappa opioid agonists such as dynorphin A-(1-13) improved amnesia induced by ischemia, basal forebrain-lesion or scopolamine. It appears that opioid receptors are fully involved in the neural basis of behavioral responses.
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PMID:[Opioid receptors in the brain related to behavior]. 823 43

The development of tolerance to morphine analgesia in amnesic model mice and the role of arginine vasopressin (AVP) in the underlying mechanism was examined. Hypoxia, brain ischemia, scopolamine and electroconvulsive shock (ECS) manipulation caused amnesia in the step-through type passive avoidance learning test performed at 24 h after the training trial. The amnesic state lasted for at least 3 days and recovered to naive control level on the 20th day after each manipulation. In all amnesic groups, radioimmunoassayable AVP content in hypothalamus was decreased, in particular, the reduction was significant in hypoxia and ischemic induced amnesic animals, then recovered to the control level by 20 days after each treatment. Daily morphine, 10 mg/kg, s.c. easily resulted in the development of tolerance to the analgesic effect in control animals; however, such treatment failed to develop tolerance in amnesic model animals, leaving the analgesic effect unchanged to the control levels. Daily pretreatment with i.c.v. AVP, dose-dependently reinstated the development of tolerance in amnesic model mice. When morphine injection was started from 20 days after the amnesia inducing treatment, tolerance developed as in a similar pattern as in control animals. Thus, amnesic model mice are deficient in brain AVP levels, and consequently, a certain level of AVP in the hypothalamus is required for maintaining the normal function such as the development of tolerance to morphine and the recovery from amnesia.
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PMID:Lack of the development of morphine tolerance in experimental amnesia: role of arginine vasopressin. 850 24

Neurocognitive dysfunction is a common sequela of cranial irradiation that is especially severe in young children. The underlying mechanisms of this disorder have not been described. The present review describes the role of the hippocampus and the anatomically related cortex in memory function and its marked susceptibility to ischemic and hypoxic injury. Based on studies of animal models of human amnesia and histopathological findings in the irradiated brain, the neurocognitive sequela of cranial irradiation can be seen to be mediated through vascular injury, resulting in ischemia and hypoxia in the hippocampal region. Recognition of the site and mechanisms of this injury may lead to the development of techniques to minimize the risks.
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PMID:Pathogenesis of irradiation-induced cognitive dysfunction. 893 10

Dural arteriovenous fistula (AVF) of the anterior cranial fossa is associated usually with cerebral hemorrhage or subarachnoid hemorrhage, while an association with transient global amnesia has not been reported previously. A case presenting the latter unusual symptom is described and the surgical treatment of AVF is discussed. A 64-year-old woman was hospitalized complaining of transient memory impairment. Magnetic resonance (MR) imaging demonstrated a flow void in the left frontal lobe and temporal pole. Cerebral angiography revealed an AVF in the anterior cranial fossa, which was fed bilaterally by the ethmoidal arteries and by branches of the external carotid arteries. The AVF drained into the superior sagittal sinus and the superficial sylvian vein via large varices. Following transfemoral embolization, surgical treatment was carried out. Postoperative angiography revealed complete obliteration of the anomaly. There were no further episodes of amnesia. In our presented case, there is an association between the presenting symptoms and the AVF. The combination of ischemia and congestion in the frontal and temporal lobes may have caused transient memory impairment. From our surgical experience, the excision of the vascular connection between the dura and the frontal lobe following the coagulation of the dura mater of the anterior part of the base of the skull without extensive excision seems to be recommended.
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PMID:Transient global amnesia and dural arteriovenous fistula of the anterior cranial fossa. 894 42

The long-standing notion that damage restricted to the hippocampal formation is sufficient to produce a significant global memory deficit derives from clinical data. Specifically, it is based on the observation that transient global ischemia, which leads to partial cell loss within the hippocampal formation but not in other brain areas important for memory, can produce global amnesia in humans. This view is, however, challenged by a number of experimental findings. First, in both monkeys and rats, there is evidence that ischemia disrupts delayed object recognition, a memory process found to be largely intact following selective hippocampal lesions. These findings indicate that damage confined to the hippocampal formation cannot account for all aspects of the ischemia-induced memory impairments. Second, although some groups of hippocampal neurons are the most prone to degeneration following ischemia, a wide array of extra-hippocampal damage has been observed in all species, for which the precise extent and distribution may well be underestimated by conventional histological evaluations of ischemic brains. Partial neuronal degeneration reported in regions such as the rhinal areas, medial dorsal thalamic nucleus, or cingulate cortex may contribute to varying degrees to ischemia-induced memory deficits. Third, experimental studies have failed to generate a general consensus on the correlation between extent of hippocampal cell loss and memory performance. In sum, the experimental studies do not, as yet, support the view that hippocampal damage is solely responsible for ischemia-induced memory deficits. Rather, they suggest that both the intra- and extra-hippocampal damage contribute to the pattern of memory impairments observed following ischemia. Consequently, although animals with global and focal ischemia represent valuable models for neuropathological and therapeutic studies, they may not be so useful in assessing the role of the hippocampal formation and its sub-components in memory processes.
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PMID:Cerebral ischemia: are the memory deficits associated with hippocampal cell loss? 895 8

1. Although the physical nature of sigma (sigma) receptors have not yet been fully defined, several classes of selective ligands have been characterised, demonstrating a plethora of physiological actions. In the present review, the authors have set out to highlight two important aspects of the biological activities of sigma ligands, their neuroprotective and anti-amnesic effects. 2. The sigma ligands present a therapeutic potential as neuroprotective agents in brain ischemia. The neuroprotective activity of many non-selective sigma ligands is primarily a result of their affinity for the NMDA receptor complex. However, selective sigma ligands are also neuroprotective, possibly by inhibition of the ischemic-induced presynaptic release of excitotoxic amino acids. 3. The sigma 1 ligands prevent the experimental amnesia induced by muscarinic cholinergic antagonists at either the learning, consolidation or retention phase of the mnesic process. This effect involves a potentation of acetylcholine release induced by sigma 1 ligands selectively in the hippocampal formation and cortex. 4. The sigma 1 receptor ligands also attenuate the learning impairment induced by dizocilpine, a non-competitive antagonist of the NMDA receptor, and may relate to the potentiating effect of sigma 1 ligands on several NMDA receptor-mediated responses previously described in vitro and in vivo in the hippocampus. This effect is shared by NPY- and CGRP-related peptides and by neuroactive steroids, confirming the in vitro evidences of functional interactions between the sigma 1 receptors and these different systems. 5. Additional amnesia models also seem to be alleviated by sigma 1 ligands, such as phencyclidine-induced cognitive dysfunctions, and amnesia induced by the calcium channel blocker nimodipine, or by exposure to carbon monoxide. Furthermore, a preliminary study in an animal model of age-related memory deficits, the senescence-accelerated mouse, strengthened the therapeutic potentials of selective sigma 1 receptor ligands in aging-related pathologies.
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PMID:Neuroprotective and anti-amnesic potentials of sigma (sigma) receptor ligands. 907 59

The neuroprotective effects of GTS-21 [3-(2,4-dimethoxybenzylidene)-anabaseine dihydrochloride] were studied and compared with those of nicotine, 9-amino-1,2,3,4-tetrahydroacridine hydrochloride hydrate (THA) and pentobarbital-Na (PB) using a cerebral ischemia model in Mongolian gerbils. The learning performance and memory retention were elucidated by a step-through passive avoidance task at 2 and 3 days after ischemia-reperfusion. In this task, the ischemia-operated gerbils showed impairment of learning performance and memory retention. Neuronal cell death in the hippocampal CA1 area was observed at 7 days after ischemia. When administered i.p. 30 min before ischemia, GTS-21 (5 mg/kg), (-)-nicotine (1.5 mg/kg), THA (5 mg/kg) and PB (50 mg/kg) significantly attenuated the impairment of passive avoidance performance and the neuronal cell death induced by the ischemia. When administered orally twice daily for 2 weeks prior to the ischemia, GTS-21 (10 mg/kg) significantly suppressed both amnesia and neuronal cell death, while (-)-nicotine (10 mg/kg) and THA (10 mg/kg) suppressed only the amnesia. These results suggest that GTS-21 exerts a protective activity on not only impairment of learning and memory but also delayed neuronal death and that the underlying mechanism of GTS-21 differs from that of nicotine or THA.
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PMID:Protective effect of GTS-21, a novel nicotinic receptor agonist, on delayed neuronal death induced by ischemia in gerbils. 951 1

1. The amnesia induced by various stress stimuli through hypoxia and cerebral ischemia was evaluated by the shortening of the response latency in a step-through task in mice. 2. The hypoxia-induced amnesia was reduced by cromakalim, a K+ channel opener (KCO), given 10 min before or immediately after the hypoxic treatment. 3. Similarly, the ischemia-induced amnesia was also reduced by cromakalim given 30 min before the occlusion. 4. In ischemic-induced amnesic mice, pyknotic cells, indicating the condensation of chromatin, were observed histochemically at the dentate gyrus granule cells in hippocampal regions 96 hr after ischemic treatment. In addition, cromakalim inhibited the induction of pyknotic cells. 5. These results suggest that KCOs might produce prophylactically neuroprotective effects against hypoxia- and cerebral ischemia-induced amnesia.
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PMID:Antiamnesic action of cromakalim, a potassium channel opener, in mice treated with hypoxia- and cerebral ischemia-type stress stimuli. 961 98

The effect of Ginkgo biloba extract (GbE) on cerebral ischemia induced by 10-min bilateral occlusion of the carotid arteries in mice was studied. Severe impairment of memory was apparent when the passive avoidance test was carried out 48 hr after bilaterally induced ischemia. When GbE at doses of 50 and 100 mg/kg was given p.o. 1 hr before the 10-min occlusion, there was a significant improvement in memory. The i.p. injection of ifenprodil (30 mg/kg) also showed improvement on learning tasks. The p.o. administration of flavonoid, a fraction isolated from GbE, showed high step-through latency on scopolamine-induced amnesia. All these findings indicate that GbE is beneficial for clinical use in amnesia accompanied with cerebral vascular disease.
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PMID:Effects of ginkgo biloba extract on impairment of learning induced by cerebral ischemia in mice. 979 64


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