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

We present a patient with transient global amnesia (TGA) whose diffusion-weighted MRI (DWI) showed increased signal in the splenium of the corpus callosum and in the left parahippocampal gyrus. The absence of high signal on the corresponding apparent diffusion coefficient (ADC) images supports the diagnosis of an acute infarction. This finding provides a temporal relation between cerebral ischemia and infarction in the territory of posterior cerebral artery and in certain cases of TGA. An early means of detecting ischemia in TGA by DWI may influence clinical decisions made in patient evaluation and management.
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PMID:Diffusion-weighted MRI characterizes the ischemic lesion in transient global amnesia. 1040 77

A variety of transient focal neurological signs presenting at high altitude have been described without associated acute mountain sickness or other concurrent illness. We report a case series of transient global amnesia at high altitude. The term high-altitude global amnesia (HAGA) is introduced to indicate this condition, and the pathophysiology is discussed. We hypothesize that because of the highly variable ventilatory response to hypoxia and to individual cerebral vasomotor reactivity, individuals with a marked hyperventilatory response could experience significant hypocapnic cerebral vasoconstriction that in turn could cause local hypoxia or ischemia to particular regions of the brain and resulting transient focal neurological impairment.
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PMID:High-altitude global amnesia. 1073 4

The transitory memory disturbance known as transient global amnesia (TGA) remains an enigma from a pathogenic point of view. In spite of its typical benign prognosis, TGA is a frightening experience for patients and their relatives. Moreover, a TGA episode usually leads to extensive investigation of patients in search of organic alterations that might be responsible for the event. Finally, TGA generates queries about therapeutic choices. In this review, we critically re-evaluate the evidence in support of and against the three main pathogenic hypotheses (i.e. ischemia, seizure discharge, and migraine), and we conclude that none of these appears completely convincing. Given the good prognosis and the lack of association with organic and instrumental abnormalities, we advance the hypothesis that TGA may be related to psychological disturbances causing transient alteration in brain metabolism and, consequently, amnesia. Our conclusion has relevant consequences in the evaluation of patients with TGA.
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PMID:Transient global amnesia: a review emphasizing pathogenic aspects. 1108 3

Ischemia has been proposed as a cause of transient global amnesia (TGA), but proof has been lacking. The authors performed magnetic resonance imaging on a 77-year-old woman with classic TGA at 4 hours and at 6 days after the onset of symptoms. Her initial diffusion-weighted imaging (DWI) and apparent diffusion coefficient imaging suggested an acute infarct in the left mesial temporal lobe. Follow-up T2-weighted imaging at 6 days confirmed the lesion as an ischemic infarct, despite resolution of her symptoms. DWI permits early detection of small ischemic lesions and may identify patients with ischemic TGA who should be evaluated for potential sources of emboli.
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PMID:Unilateral temporal lobe stroke causing ischemic transient global amnesia: role for diffusion-weighted imaging in the initial evaluation. 1146 2

The etiology of Transient Global Amnesia (TGA) is still obscure. Diffusion-Weighted-Imaging (DWI) provides conflicting evidence concerning a possible vascular ischemic cause in mesiotemporal structures including the hippocampal region. The question remains open whether conflicting observations resulted from different observation times. DWI was performed at a time interval with known sensitivity for detection of ischemia. Ten patients (5 male, 5 female; mean age of 63 +/- 9, range 41-71 years) with typical TGA were investigated at an average delay of 18 hours (range 6 to 44 hours) between onset of symptoms and magnetic resonance imaging (transversal DW-, T1W- and T2W-MRI). Five patients received apparent-diffusion-coefficient (ADC)-mapping. Cerebrovascular studies (ECG, TTE and extra/transcranial dopplersonographic and duplexultrasonic investigation) and EEG were normal in all patients. DW-MRI-sequences and ADC-maps, if performed, were normal in all patients. Conventional T2W-MRI in 3 out of 10 patients showed microangiopathic subcortical changes and lacunar strokes of older origin. We conclude that TGA does not result from a vascular ischemic etiology in the majority of cases.
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PMID:Transient Global Amnesia. Evidence against vascular ischemic etiology from diffusion weighted imaging. 1242 91

The pathogenesis and localization of neuronal dysfunction in transient global amnesia (TGA) is still disputed more than 40 years after the first description of this clinical entity. Previous studies have indicated that structural abnormality is rare in TGA. We report a case of TGA in a patient with acute ischemia in the body of right caudate nucleus. This provides evidence in support of an ischemic hypothesis as the possible etiology of TGA. The role of caudate nucleus in human memory is also reviewed.
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PMID:Transient global amnesia in a patient with acute unilateral caudate nucleus ischemia. 1526 Dec 50

To assess whether platelets are activated in transient global amnesia (TGA) and TIA, blood samples were analyzed by fluorescence-activated cytoscan using antibodies specific for platelet fibrinogen receptor (PAC1) and P-selectin (CD62P). Samples from TIA contained high levels of CD62P compared with age-matched control subjects, whereas those from TGA did not. The authors suggest that activated platelets are involved in brain ischemia, whereas ischemia appears not to be associated with most TGA.
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PMID:Activated platelets in transient global amnesia and TIA. 1532 57

Transient global amnesia is a benign syndrome of sudden-onset alteration of behavior with temporary dysfunction of anterograde and recent retrograde memory. Its neural substrates remain uncertain. Possible causes include ischemia, migraine, and epilepsy. The authors report a case of a 62-year-old man with a transient attack of memory disturbance, suggestive of transient global amnesia, in which magnetic resonance imaging performed 48 hours after onset showed left mesial temporal lobe signal changes on diffusion-weighted imaging and fluid-attenuated inversion recovery images. The findings and a literature review lend further support to the ischemic pathogenesis of transient global amnesia as a possible etiology, and underscore the role of diffusion-weighted imaging in the diagnosis of this condition.
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PMID:Evidence of acute ischemic tissue change in transient global amnesia in magnetic resonance imaging: case report and literature review. 1574 36

Transient global amnesia (TGA) is a disorder of unknown aetiology, characterized by sudden loss of anterograde memory, in the absence other neurological signs or symptoms, followed by complete recovery in less than 24h. Precipitating actions such as strenuous physical activity or valsalva-like manoeuvres are frequently reported. Since first described in 1958, by Fisher and Adams, the possible pathophysiology has undergone much speculation. Nonconvulsive epileptic seizures, migraine, paradoxical embolism thorough a patent foramen ovale, and transient ischemic attacks have been proposed as potential mechanisms. One of the latest hypotheses is that venous congestion causes either ischemia or induces spreading depression in the medial temporal lobes. It has been demonstrated that retrograde flow in the internal jugular veins occurs more frequently during valsalva manoeuvres in TGA patients than in controls, supporting a dysfunctional venous circulation as part of the pathogenesis. However, earlier hypotheses typically fail to explain the relatively low recurrence rate of TGA, lack of comorbidity and the relation to precipitating events. If cerebral venous hypertension was the solely cause of TGA it would presumably be much more common with very high recurrence rates among those predisposed of the condition. Structural changes observed in MRI and SPECT studies along with reports of mild cognitive impairment lasting much longer than the amnestic episodes, indicate that TGA is less transient and perhaps somewhat less benign than earlier believed. Many cases of TGA seem to be associated with factors of increased risk of cerebral venous thrombosis, such as polycythemia, antiphospholipid antibodies, venous hypertension, female sex and more. We suggest that most cases of TGA may be due to small thrombi in the deep cerebral venous system. Small venous thrombi may difficult to visualize even when using modern imaging technology. Further studies of TGA patients with for example blood analysis of D-dimer together with MR venography or CT venography could be done to evaluate this new hypothesis.
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PMID:Transient global amnesia may be caused by cerebral vein thrombosis. 1606 28

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


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