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Query: UMLS:C0233794 (memory impairment)
 7,237 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

28 patients with transient global amnesia (TGA) were followed for a mean period of 73 months. The patients fell into 3 diagnostic groups: a group where patients had associated symptoms and signs of transient focal cerebral ischemia (TIA), a migraine group and a miscellaneous group. 22 patients had evidence of cerebrovascular disease or risk factors for cerebrovascular disease, and a vascular basis for the amnesic attack was highly suggestive in 25 patients. During the follow-up period 2 patients died, 3 had recurrent TGA and 13 developed a completed stroke or suffered from further TIA's. Permanent memory impairment was encountered in 9 cases. An unfavourable course was related to the presence of other TIA manifestations and/or risk factors for cerebrovascular disease. The study indicates that TGA is probably due to transient ischemia in the vertebrobasilar arterial distribution area. TGA per se has a good prognosis, but the coexistence of risk factor or manifest cerebrovascular disease implies a high rate of a subsequent completed stroke or permanent memory impairment.
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PMID:Transient global amnesia -- its clinical and pathophysiological basis and prognosis. 721 Nov 87

This study examines the effect of the psychotropic drug minaprine on memory impairment in Mongolian gerbils subjected to a 5-min bilateral common carotid artery occlusion, as assessed by their performance in an 8-arm radial maze task. Gerbils were initially trained on the 8-arm radial maze until their mean error was 0-1 for 5 days. This task was repeated before the ischemia was performed and again 7 days after it. Then the animals were immediately sacrificed for histopathological examination. Severe memory impairment occurred in the control gerbils; whereas when minaprine 75 mg/kg was given orally 30 min before the 5-min occlusion, memory impairment was significantly reduced. Histopathological analysis of the control gerbils showed nearly complete loss of the pyramidal neurons in the CA1 region of the hippocampus, whereas the minaprine-treated gerbils showed complete preservation of the pyramidal neurons. These findings suggest that minaprine has memory-impairment-prevention and neuroprotective effects against short-term ischemia in gerbils.
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PMID:Prevention by minaprine of ischemic neuronal damage and memory impairment in Mongolian gerbils. 779 20

Middle aged rats (13 months) were subjected to chronic cerebrovascular insufficiency (CVI) for 9 weeks using a 3-vessel occlusion technique. This CVI injury targets CA1 neuron damage selectively. Three groups of rats had their cerebral blood flow restored after 1, 2 or 3 weeks following CVI by removal of their carotid artery occluders. Another rat group did not undergo deocclusion for the 9 week observation period. Rats were tested for memory acquisition and retention 6 and 9 weeks after CVI using a modified water maze test. At the end of the 9 weeks, cerebral blood flow was measured in the fronto-parietal cortex and rats were killed by fixation-perfusion. Hippocampal morphometry was done to assess the % of damaged CA1 neurons and the density of GFAP-positive hyperplasia and hypertrophy. Results show that restoration of cerebral blood flow 1 and 2 weeks after CVI but not after 3 weeks of CVI, reversed a significant increase in reactive astrocytosis and prevented memory impairment in these deoccluded rats when compared to the non-deoccluded group. It appears from these results that 'neuronal rescue' of CA1 neurons is possible when cerebral blood flow is restored in rats subjected to chronic CVI during a 2 week (but not 3 week) 'window of opportunity'. This chronic brain ischemia model may be useful in screening potential therapy in patients with dementia where spatial memory impairment and hippocampal damage may be manifested.
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PMID:Brain blood flow restoration 'rescues' chronically damaged rat CA1 neurons. 822 Oct 94

When rats were trained preoperatively with a three-panel runway task and were then exposed to 10-min ischemia by the method of 4-vessel occlusion, they showed no increase in the number of errors (attempts to pass through two incorrect panels of the three panel-gates at four choice points), having normal retention of memory performance learned before the ischemic insult. Next, we investigated the abilities of ischemic rats to acquire the three-panel runway task and to learn a subsequent reversal task, where the correct panel-gate locations were changed. Rats with 5-min ischemia exhibited performance as good as that of control rats, but rats exposed to 10- and 20-min ischemia showed more errors than control rats during 10 acquisition sessions and 5 subsequent reversal sessions, each of which (consisting of 6 trials) was given once a day. Marked neuronal degeneration was observed in the hippocampal CA1 sector from the rats with 10- and 20-min ischemia. Exposure to sublethal 5-min ischemia followed by 10-min ischemia at a 2-h interval had no effect on either the memory impairment during acquisition and reversal tests or the hippocampal CA1 damage. When rats were exposed to 5-min ischemia 2 days before lethal 10-min ischemia, they showed acquisition and subsequent reversal learning as good as that of control rats. Preconditioning with sublethal 5-min ischemia followed by 2 days of reperfusion also prevented the neuronal destruction of the hippocampal CA1 sector induced by 10-min ischemia. These findings suggest that postischemic hippocampal CA1 neuronal damage does not affect retention of spatial memory acquired before ischemia, but produces a significant impairment of acquisition and subsequent reversal learning. The present results also demonstrate that preconditioning with sublethal ischemia can develop tolerance to subsequent lethal ischemia to prevent the learning impairment related to the hippocampal CA1 neuronal damage.
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PMID:Ischemic tolerance to memory impairment associated with hippocampal neuronal damage after transient cerebral ischemia in rats. 873 85

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

We investigated the effect of N-benzyloxycarbonyl-thioprolyl-thioprolinal-dimethylaceta l (ZTTA), a novel postproline cleaving enzyme (prolyl endopeptidase, PPCE) inhibitor, on the in vitro activity of rat brain PPCE and memory impairment induced by cerebral ischemia. ZTTA noncompetitively inhibited rat brain PPCE (ki = 2.9 microM). Cerebral ischemia for 5 min increased the number of errors in a working memory task with a three-panel runway paradigm. ZTTA at 6 mg/kg, administered immediately after blood flow reperfusion, significantly reduced the increase in working memory errors expected to occur 24 h after 5 min of ischemia. The antiamnesic action of ZTTA may be ascribable to a neuroprotective effect on the central nervous system due to some neuropeptides that are substrates of PPCE in the brain.
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PMID:ZTTA, a postproline cleaving enzyme inhibitor, improves cerebral ischemia-induced deficits in a three-panel runway task in rats. 895 74

Studies in humans and monkeys have identified structures in the medial temporal lobe essential for memory (the hippocampal region, i.e., the dentate gyrus, the hippocampus, and the subicular complex, and the adjacent perirhinal, entorhinal, and parahippocampal cortices). Additional work has revealed that for both species, damage limited to the hippocampal region produces less severe memory impairment than damage that includes additional structures within the medial temporal lobe. This work has been based on both neurosurgical lesions and on lesions produced by global ischemia or anoxia. An important issue about ischemic damage is whether the damage identifiable in histopathological examination provides an accurate estimate of direct neural damage or whether additional direct damage might be present that is sufficient to disrupt neuronal function in areas important for memory and sufficient to impair behavioral performance, but not sufficient to progress to cell death and to be detectable in conventional histopathology. This commentary explores the issue of ischemic damage and memory impairment. Although few studies have addressed this issue directly, the currently available data from global ischemia in rats, monkeys, and humans are consistent with the hypothesis that the detectable neuronal damage is responsible for the severity of the observed behavioral impairment. Yet it is also true that this hypothesis has not been the target of very much systematic work. We encourage additional experimental work, especially in rats, that could further illuminate how to evaluate the behavioral effects of ischemic lesions.
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PMID:Ischemic brain damage and memory impairment: a commentary. 895 7

The effects of chronic cerebrovascular ischemia on memory function and cytochrome oxidase (CO) activity were investigated. Cerebrovascular insufficiency was induced by permanent bilateral carotid artery ligation (2-VO) in 19 month old rats. Sham surgery in no-vessel occlusion (no-VO) rats were used for controls. Memory function was tested 1 week prior to surgery and then weekly for 21 days using the Morris water maze. Regional brain activity of CO was measured 4 weeks after surgery by quantitative histochemistry. Histologic examination of brain slices was used to evaluate any neuropathology present. Results showed that 2-VO rats were significantly impaired in the water maze task at each testing period with respect to no-VO controls. In addition, CO activity in 2-VO rats was markedly reduced only in the dorsal CA1 region of the hippocampus and in the posterior parietal cortex. These brain regions are involved in visuo-spatial memory mechanisms. Analysis of other brain regions in 2-VO rats did not reveal further CO activity changes. There were no damaged or loss of neurons in 2-VO or no-VO groups in any region examined, including CA1 and posterior parietal cortex. The CA1 region however, is known to undergo neuronal loss 25 weeks after chronic 2-VO suggesting that this vascular insult can induce a slowly-evolving cascade consisting of neuronal damage, atrophy and death. The present findings indicate that reduced CO activity in CA1 and posterior parietal regions can predict neural damage and atrophy prior to structural perikaryal pathology following chronic brain ischemia. In addition, the data shows that neuronal energy metabolic deficiency may initiate visuo-spatial memory impairment in this aging rat model.
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PMID:Reduced cytochrome oxidase and memory dysfunction after chronic brain ischemia in aged rats. 908 Apr 58

Ischemic stroke causes various functional deficits in the brain such as memory impairment, and clinical reports have shown that the impaired brain functions may partially recover. However, there has been no experimental model suitable for studying cellular mechanisms of functional recovery following brain ischemia. Therefore, we investigated the long-term influence of transient forebrain ischemia on excitatory synaptic transmission in the rat dentate gyrus, a brain region relatively resistant to ischemia. Fifteen minutes of transient forebrain ischemia produced no apparent histological damage in dentate granule cells, but caused a significant reduction of basal synaptic potentials evoked by perforant path stimulation. Field excitatory postsynaptic potential remained reduced for at least 1 month after ischemia, while population spike recovered to control level in 1 month. The induction of long-term potentiation was also impaired after ischemia, but it showed faster recovery than basal synaptic potentials. In conclusion, we found that synaptic transmission in the dentate gyrus of the rat is impaired following transient forebrain ischemia, but has a potential to recover. These results may provide a good model for studying the mechanisms of impairment and recovery of brain function after transient ischemia.
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PMID:Early impairment and late recovery of synaptic transmission in the rat dentate gyrus following transient forebrain ischemia in vivo. 966 2


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