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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Transient global amnesia (TGA) is an unusual form of the amnestic syndrome, clinically characterized by profound disturbance of short-term memory with preservation of immediate recall and long-term memory. Spontaneous recovery is the rule and is usually complete within several hours. The etiology of TGA is not clear. It is considered to be caused by transient ischemia confined to the medial temporal lobe, an area supplied by branches of the vertebrobasilar system. Basilar artery migraine is a well-known syndrome, first described by Bickerstaff. Besides pulsating headache, the dominant symptoms are vertigo, ataxic gait, tinnitus, dysarthria, paraeshesia in the hands, homonymous hemianopsia and sometimes drop-attacks. These symptoms are associated with vertebrobasilar system dysfunction. In this paper, three migraine patients, suffering from one episode of TGA, were reported. All patients were women. Case 1 was a 48-year-old woman with a history of common migraine. Case 2 was a 48-year-old woman with a history of classic migraine. Case 3 was a 59-year-old woman with a common migraine. Family history of migraine exists in case 1 and case 3. Their migrainous attacks began in their twenties and thirties. They suddenly suffered migraine with the symptoms of vertebrobasilar dysfunction. These symptoms are ataxic gait (Case 1, 2, 3), dysarthria (Case 1, 2), vertigo (Case 1, 3) and homonymous hemianopsia (Case 1, 3). Simultaneously three patients had TGA. Duration of retrograde amnesia were about twenty-four hours (Case 1), about thirty minutes (Case 2) and about three hours (Case 3).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Basilar artery migraine associated with transient global amnesia]. 262 11

Two rat models of memory impairment in passive avoidance learning induced by cerebrovascular disturbance, were established to estimate the effects of a cerebral metabolic enhancer, idebenone. Transient and global cerebral ischemia in rats, produced by 4-vessel occlusion for 200 s immediately after the acquisition trial of passive avoidance learning, shortened the latencies in the retention test trial performed 24 h later. This retrograde amnesia was reversed significantly by idebenone administered orally or intraperitoneally at the doses of 10 and 30 mg/kg before the retention test trial. Idebenone at a dose of 10 mg/kg, given intraperitoneally before or immediately after the ischemia, also markedly inhibited the appearance of amnesia. In the second model, permanent and cerebral hemisphere embolization produced by injecting 2,000 microspheres into the internal carotid artery, significantly impaired passive avoidance learning performed 7 days later. The repeated administration of idebenone (30 mg/kg, i.p.). once a day after the embolization, significantly improved the impairment of passive avoidance learning in the embolized rats. Furthermore, physostigmine and arginine-vasopressin as reference compounds improved the impairment of passive avoidance learning in these models. These findings suggest that idebenone ameliorates memory impairment induced by cerebral vascular disturbance in rats.
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PMID:Effects of idebenone on memory impairment induced in ischemic and embolization models of cerebrovascular disturbance in rats. 276 39

The phenomenon of retrograde amnesia has important implications for understanding normal memory as well as its neural organization. Using 6 tests of remote memory, we evaluated the extent and severity of retrograde amnesia in 2 groups of amnesic patients--7 patients with alcoholic Korsakoff's syndrome and 5 other patients with amnesia (anoxia or ischemia, N = 3; thalamic infarction, N = 1; unknown etiology, N = 1). Although there were individual differences, Experiment 1 showed that the severity and extent of retrograde amnesia was similar for the 2 groups. Retrograde amnesia was temporally graded across a period of about 15 years and was not detectable in more remote time periods. In Experiment 2, repeated testing during a 3 year period showed that amnesic patients and control subjects were similarly consistent in their responses. Amnesic patients did not catch up to control subjects by eventually accumulating as many correct answers as the control subjects. In Experiment 3, amnesic patients performed normally on a test of very difficult general information questions, which were based on material likely to have been learned long ago. In all 3 experiments, the 2 groups of amnesic patients performed similarly. The results support the following conclusions: (1) Extensive, temporally graded retrograde amnesia, which has been observed frequently in patients with Korsakoff's syndrome, occurs readily in other amnesic patients as well, even when their memory impairment appears well circumscribed; (2) patients with presumed damage to either the medial temporal or the diencephalic brain structures linked to memory functions can produce a similar kind of retrograde amnesia; (3) the impairment reflects a loss of usable knowledge, not simply difficulty accessing an intact memory store that can then be overcome given sufficient retrieval opportunities; (4) very remote memory, at least for factual information, can be intact in amnesia; (5) the structures damaged in amnesia support memory storage, retrieval, or both during a lengthy period of reorganization, after which representations in memory can become independent of these structures.
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PMID:The neurology of memory: quantitative assessment of retrograde amnesia in two groups of amnesic patients. 292 83

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

Neuro- and psychopharmacological effects of isopropyl-(2-methoxy-ethyl)-1,4-dihydro-2,6-dimethyl-4-(3-nitrophenyl)-3,5-pyridinedicarboxylate (Bay e 9736, nimodipine) are described using a variety of methods measuring behavior under normal conditions, under the influence of psychotropic drugs, as well as under the influence of ischemia or hypoxia. It has been demonstrated that nimodipine -- although not being very potent when measured in mg/kg -- exerts neuro- and psychopharmacological effects characterized by influences on the extrapyramidal system, aggressive defensive behavior, and chemically induced seizures. Electroencephalographical changes become evident whenever the normal equilibrium between cerebral catecholamine and cerebral serotonin levels is disturbed. When measured under the contingencies of a one trial passive avoidance paradigm, nimodipine is able to prevent the occurrence of retrograde amnesia in rodents after amnesiogenic events such as maximal electroconvulsive seizure or hypoxia. The substance prevents behavioral and electroencephalographic disturbances, elicited by a total cerebral ischemia, which is lethal in non-treated cats. It is concluded that nimodipine besides being a cerebrally vasoactive agent has psychopharmacological properties with a profile of actions hitherto unknown.
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PMID:Behavioral effects of nimodipine in animals. 720 3

We describe a series of six patients who experienced severe retrograde amnesia (five cases) or cortical blindness (one case) during selective vertebral angiography. All angiograms were obtained with the same nonionic contrast medium. Analysis of the contrast batch demonstrated no abnormalities, but investigation of the angiographic suite revealed a faulty contrast warming cabinet resulting in injection of contrast material above body temperature. The warming cabinet was withdrawn, and the complication has not recurred. We believe that these symptoms reflect ischemia caused by vertebral arterial spasm.
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PMID:Transient global amnesia and cortical blindness after vertebral angiography: further evidence for the role of arterial spasm. 761 Oct 84

A quantitative analysis of two rat syndromes of myoclonus are presented, modeling myoclonic epilepsy and postanoxic myoclonus. Like the human conditions, both of the models benefit therapeutically from drugs that act on the serotonin system. The rat model of myoclonic epilepsy is associated with a profound loss of serotonin throughout the brain (except in the striatum) and is generated by an oscillator that is synchronized around the midline. The rat model of posthypoxic myoclonus does not demonstrate a significant reduction in serotonin in any location of its brain and is generated by a non-oscillating circuit in the medulla. Although some forms of myoclonic epilepsy may benefit from serotonin drugs because they are caused by a decrease in brain serotonin, our data indicate that posthypoxic myoclonus is not caused by a decrease in the serotonergic innervation of any region of the brain. That the raphe nuclei do not degenerate after global brain ischemia was noted by C. David Marsden in a discussion of the histologic findings of three of his human cases of posthypoxic myoclonus (page 117 of reference 10) and led him to question the hypothesis that posthypoxic myoclonus was due to a loss of serotonin neurons. Our data confirm his observation in the rat, but also indicate that density of serotonin fibers and terminals throughout the brain is not reduced by the brain ischemia that produces posthypoxic myoclonus. It remains to be determined whether the physiologic responsiveness of serotonin neurons is altered by global brain ischemia and whether changes in serotonin release or serotonin receptor properties are associated with posthypoxic myoclonus. The stability of the serotonin system in posthypoxic myoclonic rats is remarkable when one considers the wide range of disorders that is produced by the prolonged brain ischemia. The inability of the most severely posthypoxic myoclonic rats to perform 7-Hz tongue protrusions indicates substantial physiologic disruption of brainstem motor function. Moreover, the posthypoxic myoclonic rat suffers from ataxia, seizures, retrograde amnesia, and impaired ability to learn. The wide spectrum of these deficits is sharply constrasted by its apparently intact serotonin system. We have identified the inferior olive as a locus that may generate the rhythmic components of tremor and myoclonus in syndromes that are truly associated with a dramatic loss of brainstem serotonin. Serotonin acts within the inferior olive to constrain its rhythmic firing. Without intraolivary serotonin, olivary neurons are predisposed to oscillate continuously, providing a substrate upon which sustained rhythmic spiking may be superimposed. It is clear that such unconstrained rhythmicity produces synchronized whole-body tremor at 10 Hz (33, 41-43). The effects of serotonin to suppress olivocerebellar rhythmicity are mediated by postsynaptic 5-HT2 receptors that reduce the magnitude of the low-threshold calcium conductance, IT. It is notable that dysregulation of this conductance has been associated with hyper-rhythmic states in the thalamus underlying cognitive disorders ranging from depression to tinnitus (49), indicating a common mechanism underlying a variety of neurologic conditions. The identification of a specific brainstem locus (inferior olive), serotonin receptor 5-HT2, and ionic current IT involved in a form of rhythmic myoclonus may provide multiple clues toward which future pharmacotherapies can be directed.
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PMID:The serotonin hypothesis of myoclonus from the perspective of neuronal rhythmicity. 1196 57

The behavioral and neurohistological protective effects of tacrolimus (FK506) were examined in rats subjected to 15-min global forebrain ischemia. Learning and memory performance were evaluated in an aversive, non-food-motivated, eight-arm radial maze. In one experiment, naive rats were rendered ischemic, and 15 days later they were tested for acquisition of a spatial task (postoperative training). In a complementary experiment, rats were trained for 8 days and then subjected to ischemia (preoperative training); 15 days later (on Day 24 of testing) they were retested for retention of cognition. FK506 (1.0 mg/kg) was given intravenously at the beginning of reperfusion, followed by doses applied intraperitoneally 6, 24, 48 and 72 h postischemia. Behavioral performance was expressed by latency to find the goal box, and number of errors. Ischemia did not affect acquisition performance. In contrast, retention of cognition was markedly impaired by ischemia, particularly working memory (P<.05-.001). This ischemia-induced, retrograde amnesia was significantly reduced by FK506 compared to vehicle alone on Day 24, as measured by latency and working memory errors (P<.025). A neuroprotective effect of FK506 was also seen on working memory, when postischemic performance was compared to that prior to ischemia (P>.05, Day 24 vs. Day 8, paired samples), in contrast to the significant, retrograde amnesia found in the ischemic, vehicle-treated group (P<.01). FK506 also significantly reduced the extent of hippocampal CA1 cell loss; however, this effect did not correlate with behavior. The present results suggest that the histological, neuroprotective effect of FK506 may be accompanied by a reduction in cognitive impairment, as assessed in a novel, non-food-motivated, eight-arm radial maze after transient, global, cerebral ischemia in rats.
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PMID:Effect of tacrolimus (FK506) on ischemia-induced brain damage and memory dysfunction in rats. 1500 73

Transient global amnesia is a clinically well defined syndrome, characterized by transient isolated epizodes of confusion with inability to acquire new data, repetitive quieries, retrograde amnesia and absence of other neurologic symptoms or signs. Eighteen patients who presented at admission the clinical picture of transient global amnesia were, after the examination, classified in three groups: patients with symptoms or signs of transitory focal ischemia, migraine group, and miscellaneous group. The transitory global amnesia in patients suffering from atherosclerotic changes of the vascular system is usually the first manifestation of transitory ischaemic attack pointing to the vascular insufficiency of the posterior cerebral regions as the cause of attack. The typical transient global amnesia is not a rare phenomenon, but it supposes the existence of the precipitating factors. Although its "pure" form is usually benign, the appearance of other factors such as cerebral neoplasms, involved in the aetiology of transient global amnesia, requires the complete clinical examination of each individual with these symptoms.
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PMID:[Transient global amnesia--possible aetiopathogenetic mechanisms]. 1629 27

We report the case of a patient with sensorimotor conversion that improved transiently during post-anoxic medial temporal ischemia inducing anterograde and retrograde amnesia. Symptoms reappeared in parallel with mnesic recovery. This case raises a hypothesis concerning the role of hippocampi and amygdalae, which are involved in emotionally-associated memory. The amnesia may have modified the patient's "self," giving her a "distant" point of view. Another hypothesis is that cerebral anoxic stress may have "reset" the cerebral network that controls behavior. These findings give clues about the mechanisms of somatoform disorder and highlight the possibility of specific therapeutic strategies to induce cognitive reappraisal of emotionally-associated experiences.
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PMID:Transient improvement in sensorimotor conversion during post-anoxic encephalopathy with bilateral medial temporal ischemia. 2293 23


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