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

The effects of Y-8894 on experimental amnesia in rats induced by transient cerebral ischemia (600 sec) according to the method of Pulsinelli and Brierley were studied using the one trial passive avoidance response and the pole climbing discrete avoidance response. All drugs were administered to the rats immediately after recirculation. The following results were obtained: 1) In the one trial passive avoidance response test, Y-8894 (2.5, 5 and 10 mg/kg, i.p.) improved significantly the decreased latency induced by the ischemia, and it was most effective at 5 mg/kg. Calcium-hopantenate (100, 250 and 500 mg/kg, i.p.) and dihydroergotoxine (5 and 10 mg/kg, i.p.) tended to increase the latency. On the other hand, physostigmine (0.025, 0.05 and 0.1 mg/kg, i.p.), a cholinesterase inhibitor, increased the latency significantly, and it was most effective at 0.05 mg/kg. 2) The pole climbing discrete avoidance response was significantly decreased by the ischemia compared with the sham operated group, and Y-8894 (5 mg/kg, i.p.) tended to improve this decreased avoidance response. 3) Y-8894 (5 mg/kg, i.p.) facilitated recovery from the changes in glycolytic metabolism, and inhibited the accumulation of choline due to the dysfunction of the neuronal membranes induced by the ischemia. These results show that Y-8894 has beneficial effects on experimental amnesia induced by transient cerebral ischemia.
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PMID:[Pharmacological studies on Y-8894. (VII). Effects on transient cerebral ischemia-induced amnesia in rats]. 344 14

Effects of indeloxazine hydrochloride [(+/-)-2-[(inden-7-yloxy)methyl]morpholine hydrochloride, YM-08054] on cerebral ischemia were investigated in animals. Indeloxazine prolonged the gasping duration dose-dependently in decapitated mice. Bilateral occlusion of the carotid artery for 5 min shortened the latency of step-through in passive avoidance task 4 days following ischemia in mongolian gerbils. The i.p. administration of indeloxazine was started just after the surgical operation and repeated twice a day for 4 days. Indeloxazine (2 mg/kg) significantly prolonged the latency of step-through in this amnesic model, indicating a reversal effect on the ischemia-induced amnesia. In biochemical studies, decreases in brain ATP and total adenine nucleotide levels were inhibited by indeloxazine (2 mg/kg i.p., once a day for 7 days) in four-vessel occluded rats. These findings indicate that indeloxazine possesses protective effects on cerebral ischemia presumably due, in part, to improvement of the cerebral energy metabolism.
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PMID:Protective effects of indeloxazine hydrochloride on cerebral ischemia in animals. 344 40

Transient global amnesia is a benign condition of sudden onset that resolves spontaneously. Retrograde amnesia prevents recall of events antedating the episode by hours to years, and anterograde amnesia produces the characteristic features of inability to learn new material and repetitious questioning. Laboratory investigation of these patients is generally unrewarding. Transient global amnesia is easily distinguished from amnesia caused by head trauma or transient ischemic attack, confusional state, and functional amnesia. Although transient global amnesia is most likely caused by transient ischemia of brain structures important for memory, thromboembolic cerebrovascular disease is not the cause. The patient with transient global amnesia should be treated conservatively.
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PMID:Transient global amnesia. When memory temporarily disappears. 360 46

During the past 100 years, neuropsychological testing of amnesic patients has provided a valuable method for learning about the structure and organization of normal memory. One complicating feature of this work is the fact that amnesic patients differ in terms of the pattern of their lesions and in terms of what damage is present in addition to the lesions that cause amnesia. Accordingly, as the questions asked of amnesic patients have become more sophisticated, it has become increasingly important in every group of study patients to obtain information about both the severity and the selectiveness of memory impairment. The present article considers the suitability of several memory tests and other cognitive tests for the purpose of characterizing amnesic patients. Data from these tests are presented for 10 amnesic patients (6 with Korsakoff's syndrome, 3 with amnesia owing to anoxia or ischemia, and case N.A.), who constitute our standing population of study patients, and for two control groups. Data from most of the tests are also presented for patients who were amnesic following bilateral electroconvulsive therapy. Neuropsychological descriptions of patients, which appear in the Subjects section of experimental articles, need to be expanded and standardized if published findings from one laboratory are to provide a foundation for work in other laboratories with different study patients.
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PMID:Characterizing amnesic patients for neurobehavioral study. 381 41

Cardiopulmonary arrest is a test of the brain's tolerance to global ischemia. New insights into the pathophysiology of global ischemia have led to the potential use of early prophylactic anticonvulsants, hypothermia, barbiturate coma, glucose manipulations, calcium-blocking agents, and hemodilution. A wide spectrum of neurologic sequelae may follow global ischemia, ranging from brain death, vegetative states, and impairment of higher intellectual function to syndromes of amnesia and cortical blindness, post-anoxic myoclonus, delayed leukoencephalopathy, and spinal stroke. The distinctive features of these sequelae and their pathophysiologic aspects are discussed. Special attention is given to brain death and prognostication.
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PMID:Cardiopulmonary arrest. Pathophysiology and neurologic complications. 390 62

Neuropathologic examination of two patients with dementia showed chronic bilateral medial temporal lobe ischemic damage that included the hippocampus (particularly the CA-1 region), subiculum, and amygdala. Both patients had several myocardial infarctions, and the relatively circumscribed cerebral injury may have resulted from one or more episodes of global hypoxic ischemia. Focal hippocampal injury has been associated with amnesia. The additional damage to medial temporal lobe structures may have caused the dementia.
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PMID:Dementia with bilateral medial temporal lobe ischemia. 406 76

An experimental model of amnesia induced by cerebral ischemia after one-trial passive avoidance learning was established to test the effects of a novel compound, 6-(10-hydroxydecyl)-2,3-dimethoxy-5-methyl-1,4-benzoquinone (idebenone, CV-2619), and some commonly used drugs in rats. One day after the vertebral artery was electrocauterized bilaterally, the common carotid artery was transiently occluded bilaterally to produce cerebral ischemia. The amnesia was estimated by the response latency for a rat to step from a light safety compartment to a dark compartment in which a foot-shock was given. The results of the retention test given 24 hr after the ischemia indicated that amnesia was successfully produced when the 200-600 sec ischemia was provided within 20 min after the avoidance learning. The effects of drugs on the amnesia induced by a 200-sec ischemia immediately after the avoidance learning were as follows: CV-2619 (10, 30 mg/kg, i.p. or p.o.) given before the retention test significantly increased the response latency, indicating a reversal effect on the amnesia. Physostigmine (0.1, 0.2 mg/kg, i.p.) and arginine-vasopressin (10 micrograms/kg, s.c.) were also effective, and calcium hopantenate (500 mg/kg, p.o.) showed a slight reversal action. Furthermore, CV-2619 (10 mg/kg, i.p.), given before or after the ischemia, significantly inhibited the appearance of amnesia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Beneficial effect of idebenone (CV-2619) on cerebral ischemia-induced amnesia in rats. 654 47

30 patients with acute onset of memory disturbances and visual impairment (cortical blindness or hemianopsia) are reported. For all of them, there was evidence of posterior cerebral artery ischemia. This clinical syndrome is compared with Dide and Botcazo's case report. The amnesia never recovered in 17 patients and was transient in 13 patients: in 4 of them it occurred during vertebral angiography and in 4 during general anaesthesia with anoxia. The main clinical features of the syndrome and the related bibliography are reviewed.
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PMID:[Amnesic syndrome of posterior cerebral ischemia]. 721 26

We previously reported lesions confined specifically to the hippocampus when produced by occluding eight vessels (the bilateral vertebral, common, internal, and external carotid arteries), which supply blood to the brain. However, histopathological changes in the primate brain, caused by ischemic injury, have not previously been thoroughly investigated. In the present study, macaque monkeys were subjected to 5-18-min ischemia by occluding the eight vessels. After the brains were perfused and fixed 5 days after the occlusion, all regions were histologically investigated for ischemic cell changes. Ischemia for 5 min produced no ischemic cell change. Ischemia for 10-15 min produced cell death limited to the deeper portion of the pyramidal cell layer of the CA1 subfield in the hippocampus. In most monkeys, no cell death was observed in any brain region outside of the hippocampus after ischemia for up to 15 min. Ischemia for 18 min produced more widespread cell death in the CA1 subfield of the hippocampus, and cell death was no longer confined to the hippocampus, but was observed in layers III, V, and VI of the neocortices, the striatum, and some other regions. Brains that were perfused and fixed 1 year after 15-min ischemic insult revealed no ischemic cell morphological change in any region, but the number of pyramidal cells in the CA1 subfield was decreased to about half. The results indicate that the CA1 subfield of the monkey hippocampus is the precise region of the brain most susceptible to ischemic insult in the primate forebrain, and after a critical time (15-min ischemia in this procedure) ischemic cell changes occur suddenly and extensively. Ischemia due to occlusion of eight arteries for 10-15 min could produce a model of human amnesia caused by transient ischemic insult.
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PMID:Ischemic neuronal damage specific to monkey hippocampus: histological investigation. 760 82

We have examined the effects of transient cerebral ischemia on performance of a one-trial passive avoidance task by chicks. Transient forebrain ischemia was induced by bilateral carotid artery occlusion for a period of 10 min. In one experimental group, ischemia was produced prior to training on the avoidance task whereas in the other group ischemic intervention was not made until 3 h after initial training. Sham-operated groups were matched to each of the experimental groups. All four groups were tested for retention of the avoidance response 24 h post-surgery. The sham-operated birds and those receiving post-training ischemia showed good retention of the avoidance response, whereas in birds which received ischemia prior to training there was significant amnesia. Neuronal damage, determined qualitatively using a silver impregnation method, was observed in several forebrain regions including the hippocampus, hyperstriatal regions, paleostriatum primitivum, ventral archistriatum, and lateral corticoid area. Damage was also observed in the Purkinje cells of the cerebellum. The behavioural and anatomical effects of transient forebrain ischemia have not been previously investigated in an avian species and the finding of significant amnesia for a learning task following ischemia is in good agreement with several behavioural studies in mammals.
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PMID:Transient cerebral ischemia disrupts performance on a one-trial passive avoidance task in the domestic chick and is associated with neuronal degeneration in the central nervous system. 783 91


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