Disease relevance of Ischemic Attack, Transient

• Sixty-eight patients (3.2%) developed adverse neurological events, defined as cerebrovascular accident, transient ischemic attack (TIA), or persistent coma [1].
• Questions remain regarding the discrepancy between epidemiological data and statin trials data, the precise mechanism of action of statins, and their role in the prevention of recurrent stroke in individuals who have experienced a previous stroke or transient ischemic attack but are free of coronary disease [2].
• Clonidine testing resulted in suppression of plasma norepinephrine levels but was complicated by severe hypotension and a transient ischemic attack [3].
• One transient ischemic attack and one femoral pseudoaneurysm occurred in the MVP group [4].
• Cholesterol embolism as a cause of transient ischemic attacks and cerebral infarction [5].

Psychiatry related information on Ischemic Attack, Transient

• By the use of logistic regression and propensity matching, composite neurologic outcomes (transient ischemic attack, stroke, delirium, coma, and memory deficit) were evaluated [6].
• In this longitudinal study multichannel MEG was used to localize and to quantify focal pathological spontaneous neuromagnetic activity in six patients with transient ischemic attacks (TIA) and two patients with transient global amnesia (TGA) [7].
• OBJECTIVE: To report the development of symptoms suggesting transient ischemic attacks during bupropion treatment for smoking cessation [8].
• We here report the case of a 69-year-old woman with recurrent transient ischemic attacks (TIAs) and strokes, seizures, and dementia without any mutations in exons 3 and 4 of the Notch3 gene and with a normal skin biopsy, but who showed characteristic CADASIL abnormalities on brain pathological examination [9].

High impact information on Ischemic Attack, Transient

• METHODS: We conducted a randomized, double-blind, placebo-controlled trial of estrogen therapy (1 mg of estradiol-17beta per day) in 664 postmenopausal women (mean age, 71 years) who had recently had an ischemic stroke or transient ischemic attack [10].
• For transient ischemic attacks, after carotid artery surgery has been eliminated as an option, aspirin is the drug of choice for men; for women, and for men in whom aspirin fails, warfarin sodium should be considered [11].
• High-dose corticosteroids (20 mg/kg intraperitoneally), given within 2 hours of transient cerebral ischemia, acutely increased endothelial nitric oxide synthase (eNOS) activity, augmented regional cerebral blood flow (CBF) by 40% to 50%, and reduced cerebral infarct size by 32% [12].
• Ticlopidine was first shown to decrease major events compared with placebo or aspirin in patients with stroke or recent transient ischemic attack [13].
• Surprisingly, AQP4 was strongly reduced but alpha-syntrophin was retained in perivascular astroglial end-feet in WT mice examined 23 h after transient cerebral ischemia [14].

Chemical compound and disease context of Ischemic Attack, Transient

• The Controlled trial of Aspirin in Cerebral Ischemia compared aspirin (650 mg twice daily) with placebo in medically and surgically treated groups of patients who had experienced transient ischemic attacks [15].
• Atherosclerosis potentiates constrictor responses of large cerebral arteries to serotonin and thromboxane, which may contribute to vasospasm and transient ischemic attacks [16].
• When only stroke was considered as the end point, dipyridamole and acetylsalicylic acid seemed to be more effective in reducing the risk of transient ischemic attacks than stroke, and more effective in men than in women [17].
• In a prospective study of 3,017 patients with transient ischemic attack or minor ischemic stroke from the Dutch Transient Ischemic Attack Trial, the presence or absence of diffuse hypodensity of the white matter on a baseline computed tomography (CT) scan of the brain was related to the occurrence of subsequent stroke [18].
• Stress-induced inhibition of protein synthesis initiation: modulation of initiation factor 2 and guanine nucleotide exchange factor activities following transient cerebral ischemia in the rat [19].

Biological context of Ischemic Attack, Transient

• CONCLUSIONS: These results indicate that shear-induced platelet aggregation is increased in patients with atherothrombotic stroke and transient ischemic attacks, is correlated with the increase of larger von Willebrand factor multimers, and is corrected by ticlopidine but not by low-dose aspirin [20].
• These results demonstrate that a member of the basic helix-loop-helix family of transcription factors, SEF-2, and the major subunit of the 26S proteasome complex, p112, display altered gene expression in the hippocampus after transient cerebral ischemia [21].
• Phosphorylation of extracellular signal-regulated kinase after transient cerebral ischemia in hyperglycemic rats [22].
• The ability of full and partial benzodiazepine receptor agonists to prevent DNA fragmentation and neuronal death after transient cerebral ischemia was investigated in the Mongolian gerbil [23].
• These results suggest that AQP4, but not AQP1 or AQP9, may play an important role in water movement associated with the pathophysiology of edema after transient cerebral ischemia in the mouse [24].

Anatomical context of Ischemic Attack, Transient

• BACKGROUND AND PURPOSE: Prolonged inhibition of protein synthesis precedes delayed neuronal death in the CA1 sector of the hippocampus after transient cerebral ischemia [25].
• We examined the concentrations of lactate dehydrogenase in the cerebrospinal fluid of 25 patients with strokes and 15 patients with transient ischemic attacks less than or equal to 8 hours after the onset of the vascular event and in a control group of 21 patients [26].
• We tested the in vivo activation of leukocytes by measuring plasma oxidation of adrenaline to adrenochrome in patients suffering from cerebral ischemia, cerebral hemorrhage, and transient ischemic attacks and in healthy subjects [27].
• Pravastatin reduces the risk of stroke in patients with coronary artery disease and average cholesterol levels; simvastatin reduces the risk of the combined endpoint of stroke and transient ischemic attack in hypercholesterolemic patients with coronary artery disease [28].
• Regional cerebral blood flow (rCBF) was measured over both hemispheres in 20 patients with unilateral transient ischemic attacks (TIA) of the territory of the internal carotid artery on the day of the TIA. rCBF was estimated with the nontraumatic Xenon 133-inhalation technique using the initial slope index [29].

Gene context of Ischemic Attack, Transient

• The neurons that accumulate beta/A4 amyloid protein precursor (APP) after transient cerebral ischemia were characterized by comparing their distribution with those destined to suffer delayed neuronal death or those with induction of 72-kDa heat-shock protein [30].
• Heme oxygenase-2 acts to prevent neuronal death in brain cultures and following transient cerebral ischemia [31].
• Changes in MAP2 and clathrin immunoreactivity were studied in gerbil hippocampus after transient cerebral ischemia [32].
• When comparing symptomatic vs. asymptomatic patients, the most striking finding was the coincidence between c-fos, PCNA and p53 protein positivity observed only in unstable plaques of seven out of eight patients, all with previous episodes of stroke or transient ischemic attacks [33].
• CD40/CD40L expression is elevated in patients after a transient ischemic attack or stroke [34].

Analytical, diagnostic and therapeutic context of Ischemic Attack, Transient

• BACKGROUND: Large intervention studies suggest that aspirin may reduce mortality when given to patients who present with strokes or transient ischemic attacks [35].
• SPECT study of cerebral blood flow reactivity after acetazolamide in patients with transient ischemic attacks [36].
• In a double-blind multicenter study, 124 patients with transient ischemic attacks were randomly allocated to one of two groups treated with aspirin (ASA) or sulfinpyrazone respectively [37].
• Adenosine release and changes in pial arteriolar diameter during transient cerebral ischemia and reperfusion [38].
• We report the vasocapacitance of the cerebral circulation, as determined by cerebral blood flow reactivity to induced hypercapnia using fluoromethane positron emission tomography, in 32 patients with unilateral anterior circulation transient ischemic attacks [39].

References