Gene/Protein Disease Symptom Drug Enzyme Compound
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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 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

The acute anti-ischemic and anti-anoxic effects of dextrorphan (DX) were compared with those of dizocilpine (MK-801) in a variety of animal models, and in vivo and in vitro testings under anoxic conditions. DX reduced the incidence of death in ischemic mice and improved the rotarod performance of mice with brain ischemia. The ischemically-impaired memory of mice treated with DX markedly improved, as shown in the step-through type passive avoidance test, Morris water maze and in the habituation of exploratory behavior test. MK-801 likewise improved the water maze performance of the ischemically-impaired mice, but to a lesser extent. The step-through type passive avoidance performance of ischemic mice was not improved by MK-801. In the passive avoidance task with normal mice, DX, like MK-801, produced anterograde amnesia at doses higher than those needed to attenuate the behavioral effects of ischemia. DX, intravenously or centrally administered, markedly and dose-dependently reduced the incidence of death in mice receiving potassium cyanide (KCN). DX lessened the reduction in adenosine triphosphate (ATP) and increased lactate contents in mice dosed with KCN and also lessened the reduction in ATP in the TCA cycle and oxidative phosphorylation reactions caused by KCN (0.58 mmol/l), whereas MK-801 failed to show any effect on ATP formation pathways in vivo and in vitro, and failed to protect mice against KCN-induced lethal toxicity in vivo. In the in vitro studies, DX increased the adenylate kinase activity of the rat brain homogenate. DX was found to be a cerebroprotectant with anti-ischemic and anti-anoxic actions, the effects probably stemming from its N-methyl-d-aspartate receptor antagonistic property in cooperation with its ATP replenishing action.
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PMID:Dextrorphan attenuates the behavioral consequences of ischemia and the biochemical consequences of anoxia: possible role of N-methyl-d-aspartate receptor antagonism and ATP replenishing action in its cerebroprotecting profile. 787 Sep 46

Anterograde amnesia, a common consequence of transient cerebral ischaemia, has been attributed to cell loss in the hippocampal CA1 subfield. However, variable, widespread damage outside hippocampal CA1 can also occur following ischaemia. We compared the functional consequences of ischaemia and ibotenate acid CA1 lesions on 2 spatial memory tasks (water maze 'place' and 'matching-to-position') to address the possibility that extra-CA1 loss contributes to ischaemia-induced memory deficits in the rat. During place task acquisition, ischaemic rats showed deficits on more measures than ibotenic rats, and during a 1 min probe trial, only ischaemic rats were impaired. On the matching-to-position task, ibotenic rats showed greater impairment than ischaemic rats in terms of one-trial learning, whereas ischaemic rats were more impaired after Trial 2. Ischaemia and ibotenic acid lesions resulted in equivalent CA1 loss, but silver impregnation revealed additional extra-CA1 cell loss in ischaemic rats. Together with the greater behavioural deficits of ischaemic rats, these data indicate a role for extra-CA1 cell loss in ischaemia-induced memory impairments in both animals and humans.
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PMID:Neurotoxic dorsal CA1 lesions versus 4 VO ischaemic lesions: behavioural comparisons. 1156 23

A 54-year-old diabetic, hypertensive man with poorly controlled moderate-severe sleep apnea presented with acute onset of severe anterograde amnesia and well preserved remote memory without additional cognitive impairment. Investigations, including a lumbar puncture, electroencephalogram (EEG) and serology testing ruled out infectious, neoplastic and epilleptogenic causes. MRI taken 10 days after symptom onset, was suggestive of sequential ischemic damage to both hippocampal formations. Neuropyschological evaluation suggested a focal and dense amnestic syndrome with little improvement over time. The bilateral nature of hippocampal ischemia though has been reported, is rare.
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PMID:Selective cognitive patterns resulting from bilateral hippocampal ischemia. 2229 52

Transient global amnesia (TGA) is a clinical syndrome characterized by the sudden onset of anterograde amnesia (the inability to encode new memories), accompanied by repetitive questioning, sometimes with a retrograde component, lasting up to 24 hours, without compromise of other neurologic functions. Herein, we review current knowledge on the epidemiology, pathophysiology, clinical diagnosis, and prognosis of TGA. For this review, we conducted a literature search of PubMed, with no date limitations, using the following search terms (or combinations of them): transient global amnesia, etiology, pathophysiology, venous hypertension, migraine, magnetic resonance imaging, computed tomography, electroencephalography, prognosis, and outcome. We also reviewed the bibliography cited in the retrieved articles. Transient global amnesia is a clinical diagnosis, and recognition of its characteristic features can avoid unnecessary testing. Several pathophysiologic mechanisms have been proposed (venous insufficiency, arterial ischemia, and migrainous or epileptic phenomena), but none of them has been proved to consistently explain cases of TGA. Brain imaging may be considered and electroencephalography is recommended when episodes are brief and recurrent, but otherwise no investigations are necessary in most cases. Data on long-term prognosis are limited, but available information suggests that the relapse rate is low, the risk of stroke and seizures is not considerably increased, and cognitive outcome is generally good.
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PMID:Transient global amnesia. 2593 46