salicylates and Ischemic-Attack--Transient

Aspirin is the standard treatment for secondary prevention of stroke and other vascular events. Several studies suggest that triflusal may have a better safety profile.. To determine in people at high risk of vascular events whether triflusal is an effective and safe treatment for primary and secondary prevention of serious vascular events.. We searched the trials registers of the following Cochrane Review Groups: Stroke Group (last searched October 2004), Heart Group, Peripheral Vascular Diseases Group and Metabolic and Endocrine Disorders Group (last searched May 2003). In addition, we searched the Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library Issue 2, 2003), MEDLINE (1977 to 2003) and EMBASE (1980 to 2003). We searched reference lists and contacted researchers in the field, authors of relevant trials and the drug manufacturer.. Randomised and quasi-randomised studies comparing triflusal with placebo or aspirin in people at high risk of vascular events.. Two authors independently assessed trial quality and extracted data. The primary outcome was a serious vascular event (non-fatal acute myocardial infarction (AMI), non-fatal ischemic or hemorrhagic stroke, or vascular death). Other efficacy and safety measures collected were frequency of different vascular events, adverse events, minor and major hemorrhages.. (1) Aspirin versus triflusal: five studies enrolled patients with stroke or transient ischemic attack (TIA) (4 trials; 2944 patients; followed for 6 to 47 months) or AMI (one trial; 2275 patients; followed for 35 days). Entry criteria were similar within each subgroup of patients. Patient groups were appropriately selected and well matched. The primary outcome in all trials was a composite outcome of vascular events. Trials had no important bias except in one study (217 patients). For the primary outcome of a serious vascular event there was no significant difference between triflusal and aspirin; the odds ratio (OR) was 1.04 (95% confidence interval (CI) 0.87 to 1.23). Significant differences were found for frequency of hemorrhages, both minor (OR 1.60, 95% CI 1.31 to 1.95) and major (OR 2.34, 95% CI 1.58 to 3.46) and for non-hemorrhagic gastrointestinal adverse events (OR 0.84, 95% CI 0.75 to 0.95). Sensitivity analysis of well versus poorly allocated trials showed no significant differences. (2) Triflusal versus placebo: two trials enrolled patients with unstable angina (281 patients) or peripheral arteriopathy (122 patients), who were followed for 6 months. Triflusal was associated with a reduction in serious vascular events (OR 2.29, 95% CI 1.01 to 5.19; OR greater than 1 favours triflusal) and with a higher frequency of adverse events (OR 1.68, 95% CI 1.00 to 2.80).. No significant differences were found between triflusal and aspirin for secondary prevention of serious vascular events in patients with stroke or TIA and AMI. However, our review cannot exclude moderate differences in efficacy. Triflusal was associated with a lower risk of hemorrhagic complications.

Topics: Aspirin; Humans; Ischemic Attack, Transient; Myocardial Infarction; Platelet Aggregation Inhibitors; Randomized Controlled Trials as Topic; Risk Factors; Salicylates; Stroke

The mean follow-up in the clinical trials of antiplatelet drugs in the secondary prevention of ischemic atherothrombotic stroke ranges from 1 to 5.5 years. Thus, the safety and efficacy of these drugs in the very long term is not totally documented. We have assessed the safety and effectiveness of triflusal and aspirin for a very long-term period in the secondary prevention of patients with ischemic atherothrombotic stroke.. Patients with atherothrombotic ischemic stroke, including TIA, who participated in randomized clinical trials of triflusal versus aspirin were included in the study. The period of recruitment was between 1983 and 1999. After finishing their participation in the clinical trials, patients were followed up in the Neurology Department of our hospital. All patients were treated with aspirin or triflusal during a mean period of 17.2 years. Groups were comparable with respect to sex, age, risk factor and etiology of the stroke. Adverse events and vascular events (including stroke recurrence, ischemic heart disease and vascular death) that appeared throughout the study were registered. Statistical analysis was performed using the statistical package SPSS 15.0 for Windows. Kaplan-Meier curves and the log-rank test were used to compare treatments.. A total of 441 patients (305 men) with a mean age (±SD) of 51.1±12.4 years were included in the study; 288 patients (65.3%) were treated with triflusal and 153 with aspirin. There were no statistically significant differences between aspirin and triflusal concerning new vascular events (72.5 vs. 60.4%; p=0.28), stroke recurrence (49.7 vs. 46.5%; p=0.53), ischemic heart events (54.9 vs. 55.6%; p=0.90), vascular death (25.5 vs. 24%; p=0.73) and global mortality (42.5 vs. 42%; p=0.92). The incidence of serious bleeding (upper digestive tract hemorrhage and cerebral hemorrhage) was 18.3% in aspirin-treated patients and 5.5% in triflusal-treated patients (p<0.001). In reference to other adverse events, no significant differences were found between aspirin and triflusal.. In the secondary prevention of ischemic stroke, very long-term treatment with triflusal or aspirin seems to have a similar efficacy, but triflusal is safer with a lower hemorrhagic risk. Triflusal may be an alternative therapy, particularly in patients who present aspirin resistance.

Topics: Aged; Aspirin; Brain Ischemia; Dyspepsia; Female; Follow-Up Studies; Hemorrhage; Humans; Incidence; Intracranial Arteriosclerosis; Ischemic Attack, Transient; Kaplan-Meier Estimate; Male; Middle Aged; Myocardial Ischemia; Platelet Aggregation Inhibitors; Recurrence; Salicylates; Secondary Prevention; Vascular Diseases

Triflusal is an antiplatelet agent that has shown clinical advantages when compared with aspirin in the secondary prevention of vascular events. TAPIRSS (Triflusal versus Aspirin for Prevention of Infarction: a Randomized Stroke Study) explored the efficacy and safety of triflusal in the secondary prevention of stroke in a Latin American homogeneous population with the ultimate aim of preparing for a larger trial in the same setting.. A double-blind, multicenter, randomized, pilot trial was conducted in Buenos Aires, Argentina, from October 1996 to November 1999. The study sample was 431 patients, randomized to receive aspirin 325 mg daily or triflusal 600 mg daily for a mean of 586 days. All patients had experienced either an ischemic stroke or TIA within 6 months from enrollment. Data from 429 patients were analyzed.. No differences were observed in the primary endpoint that combined the incidence of vascular death, cerebral ischemic infarction, nonfatal myocardial infarction, or major hemorrhage (aspirin 13.9%, triflusal 12.7%; odds ratio [OR] 1.11, 95% CI 0.64 to 1.94) or in the individual analysis of each component of the primary endpoint. In a post hoc analysis, the overall incidence of major and minor hemorrhagic events was significantly lower in triflusal-treated patients (aspirin 8.3%, triflusal 2.8%; OR 3.13, 95% CI 1.22 to 8.06).. This pilot trial has not found differences between triflusal and aspirin in the prevention of vascular complications after TIA or ischemic stroke, although given the wide CI, potentially important group differences could not be ruled out. Triflusal may be associated with a lower risk of hemorrhagic complications. A larger, prospective clinical trial is necessary to verify these results.

Topics: Aged; Aspirin; Cerebral Infarction; Double-Blind Method; Female; Follow-Up Studies; Humans; Ischemic Attack, Transient; Male; Middle Aged; Odds Ratio; Pilot Projects; Platelet Aggregation Inhibitors; Salicylates; Secondary Prevention; Stroke; Survival Analysis; Treatment Outcome

Glycine is a strychnine-sensitive inhibitory neurotransmitter in the central nervous system (CNS), especially in the spinal cord, brainstem, and retina. The objective of the present study was to investigate the potential neuroprotective effects of GlyT1 inhibitor N [3-(4'-fluorophenyl)-3-(4'-phenylphenoxy) propyl] sarcosine (NFPS) in the rat model of experimental stroke.. In vivo ischaemia was induced by transient middle cerebral artery occlusion (tMCAO). The methods of Western Blotting, Nissl Staining and Morris water maze methods were applied to analyze the anti-ischaemia mechanism.. The results showed that high dose of NFPS (H-NFPS) significantly reduced infarct volume, neuronal injury and the expression of cleaved caspase-3, enhanced Bcl-2/Bax, and improved spatial learning deficits which were administered three hours after transient middle cerebral artery occlusion (tMCAO) induction in rats, while, low dose of NFPS (L-NFPS) exacerbated the injury of ischaemia. These findings suggested that low and high dose of NFPS produced opposite effects. Importantly, it was demonstrated that H-NFPS-dependent neuronal protection was inverted by salicylate (Sal), a specific GlyR x0251;1 antagonist. Such effects could probably be attributed to the enhanced glycine level in both synaptic and extrasynaptic clefts and the subsequently altered extrasynaptic GlyRs and their subtypes.. These data imply that GlyT1 inhibitor NFPS may be a novel target for clinical treatment of transient focal cerebral ischaemia and reperfusion which are associated with altered GlyR alpha 1 subunits.

Topics: Animals; bcl-2-Associated X Protein; Blotting, Western; Brain; Caspase 3; Disease Models, Animal; Glycine; Glycine Plasma Membrane Transport Proteins; Immunohistochemistry; Infarction, Middle Cerebral Artery; Ischemic Attack, Transient; Male; Maze Learning; Neuroprotective Agents; Proto-Oncogene Proteins c-bcl-2; Rats; Rats, Sprague-Dawley; Receptors, Glycine; Salicylates; Sarcosine

To compare rates and predictors of documented hypoglycaemia in type 2 diabetes patients treated with either basal insulin supported oral therapy (BOT), conventional therapy (CT) or supplementary insulin therapy (SIT) in primary care.. Data from 10,842 anonymous patients (mean age ± SD: 54 ± 8 yrs) on BOT, 2,407 subjects (56 ± 7 yrs) on CT, and 7,480 patients (52 ± 10 yrs) using SIT from 1,198 primary care practices were retrospectively analyzed (Disease Analyzer, Germany: 01/2005-07/2013). Stepwise logistic regression (≥1 documented hypoglycaemia: ICD code) was used to evaluate risk factors of hypoglycemia.. The unadjusted rates (95% CI) per 100 patient-years of documented hypoglycaemia were 1.01 (0.80-1.20) (BOT), 1.68 (1.10-2.30) (CT), and 1.61 (1.30-1.90) (SIT), respectively. The odds of having ≥1 hypoglycemia was increased for CT (OR; 95% CI: 1.71; 1.13-2.58) and SIT (1.55; 1.15-2.08) (reference: BOT). Previous hypoglycemia (OR: 11.24; 6.71-18.85), duration of insulin treatment (days) (1.06; 1.05-1.07), history of transient ischemic attack (TIA)/stroke (1.91; 1.04-3.50), and former salicylate prescriptions (1.44; 1.06-1.98) also showed an increased odds of having hypoglycemia. Higher age was associated with a slightly lower odds ratio (per year: 0.98; 0.97-0.99).. Insulin naïve type 2 diabetes patients in primary care, initiated with CT and SIT have an increased risk of hypoglycaemia compared to BOT, which is in line with previous randomized controlled trials. As hypoglycaemic events are associated with an increased mortality risk, this real-world finding is of clinical relevance.

Topics: Adult; Age Factors; Databases, Factual; Diabetes Mellitus, Type 2; Drug Prescriptions; Female; Germany; Humans; Hypoglycemia; Incidence; Insulin; Ischemic Attack, Transient; Male; Middle Aged; Primary Health Care; Recurrence; Risk Factors; Salicylates; Time Factors

Topics: Aspirin; Carotid Arteries; Clinical Trials as Topic; Endarterectomy, Carotid; Guidelines as Topic; Humans; Ischemic Attack, Transient; Platelet Aggregation Inhibitors; Salicylates; Stents; Stroke

We investigated the relative contribution of COX-1 and/or COX-2 to oxidative damage, prostaglandin E2 (PGE2) production and hippocampal CA1 neuronal loss in a model of 5 min transient global cerebral ischemia in gerbils. Our results revealed a biphasic and significant increase in PGE2 levels after 2 and 24-48 h of reperfusion. The late increase in PGE2 levels (24 h) was more potently reduced by the highly selective COX-2 inhibitor rofecoxib (20 mg/kg) relative to the COX-1 inhibitor valeryl salicylate (20 mg/kg). The delayed rise in COX catalytic activity preceded the onset of histopathological changes in the CA1 subfield of the hippocampus. Post-ischemia treatment with rofecoxib (starting 6 h after restoration of blood flow) significantly reduced measures of oxidative damage (glutathione depletion and lipid peroxidation) seen at 48 h after the initial ischemic episode, indicating that the late increase in COX-2 activity is involved in the delayed occurrence of oxidative damage in the hippocampus after global ischemia. Interestingly, either selective inhibition of COX-2 with rofecoxib or inhibition of COX-1 with valeryl salicylate significantly increased the number of healthy neurons in the hippocampal CA1 sector even when the treatment began 6 h after ischemia. These results provide the first evidence that both COX isoforms are involved in the progression of neuronal damage following global cerebral ischemia, and have important implications for the potential therapeutic use of COX inhibitors in cerebral ischemia.

Topics: Animals; Antioxidants; Biomarkers; Cell Count; Cyclooxygenase 1; Cyclooxygenase 2; Cyclooxygenase 2 Inhibitors; Cyclooxygenase Inhibitors; Dinoprostone; Disease Models, Animal; Disease Progression; Gerbillinae; Glutathione; Hippocampus; Ischemic Attack, Transient; Isoenzymes; Lactones; Lipid Peroxidation; Male; Neurodegenerative Diseases; Neurons; Neuroprotective Agents; Oxidation-Reduction; Prostaglandin-Endoperoxide Synthases; Salicylates; Sulfones

Triflusal is a fluorinated aspirin derivative with antiplatelet properties, which is used in Spain for the management and prevention of thromboembolic disease.. A 91-year-old female developed a systemic photosensitivity reaction 15 days after beginning triflusal preventive treatment (300 mg/12 h) for prior transient ischaemic attack. Photobiological study showed an abnormal response to light in areas exposed to ultraviolet B and A radiation, with a photopatch test positive to both triflusal and its main metabolite. These observations suggested a causal relation between triflusal and the clinical findings, as described in previous reports.. The few cases reported to date and the clinicopathological features of this case suggested an immunological response as the most likely cause of the reaction.

Topics: Aged; Aged, 80 and over; Female; Humans; Ischemic Attack, Transient; Photosensitivity Disorders; Platelet Aggregation Inhibitors; Salicylates

Topics: Aged; Anticoagulants; Aspirin; Drug Therapy, Combination; Female; Humans; Ischemic Attack, Transient; Male; Middle Aged; Platelet Aggregation Inhibitors; Practice Patterns, Physicians'; Recurrence; Salicylates; Surveys and Questionnaires; Sweden

Selective neuronal cell death in the CA1 pyramidal cells of the hippocampus and neurons of the dorsolateral striatum as a consequence of brain ischemia/reperfusion (IR) can be ameliorated with brain hypothermia. Since postischemic injury is mediated partially by chemical production of reactive oxygen species (ROS), decreased ROS production may be one of the mechanisms responsible for cerebral protection by hypothermia. To determine if ischemic brain temperature alters ROS production, reversible IR was produced in rats by occlusion of both carotid arteries with hemorrhagic hypotension. After 15 min of ischemia, circulation was restored for 60 min. Brain temperature was maintained during ischemia at either 30, 36, or 39 degrees C and kept at 36-37 degrees C after reperfusion. Using cerebral microdialysis, we measured nonenzymatic hydroxylation of salicylate by HPLC with electrochemical detection in the hippocampus. CBF was also compared among the groups during IR. The results were that normothermic animals during reperfusion had persistently increased levels of the salicylate hydroxylation product, 2,3-dihydroxybenzoic acid (2,3-DHBA), reaching 251% of control at 60 min. This increase in 2,3-DHBA production was potentiated after 60 min of reperfusion (406% of control) with ischemic hyperthermia. In hypothermic ischemia, 2,3-DHBA production at 60 min was attenuated to 160% of control. CBF decreased to approximately 5% of baseline value during ischemia, but increased three- to four-fold relative to control in all three groups. Therefore, the effects of ischemic brain temperature on 2,3-DHBA production did not correlate with changes in CBF during IR. We conclude that brain-temperature-related changes in OH.production are readily detected in the rat and decreased ROS generation may contribute to cerebral protection afforded by hypothermia during brain ischemia.

Topics: Analysis of Variance; Animals; Body Temperature; Brain; Cerebral Cortex; Cerebrovascular Circulation; Chromatography, High Pressure Liquid; Free Radical Scavengers; Hippocampus; Hydroxybenzoates; Hydroxyl Radical; Hydroxylation; Iron Chelating Agents; Ischemic Attack, Transient; Laser-Doppler Flowmetry; Male; Microdialysis; Rats; Rats, Sprague-Dawley; Reperfusion Injury; Salicylates; Salicylic Acid

Using the microdialysis technique and laser-Doppler flowmetry, we performed simultaneous measurement of salicylate hydroxylation and glutamate release along with local CBF in the ischemic penumbral cortex of rat brain subjected to normothermic transient middle cerebral artery (MCA) occlusion. Cortical CBF fell to 24 +/- 11% (mean +/- SD) during ischemia and recovered to 84 +/- 16% during reperfusion. Extracellular glutamate levels increased by 6.5-fold above baseline 10 min following MCA occlusion but subsequently returned to near baseline levels in spite of the persistent ischemia. Increase in 2,3- and 2,5-dihydroxybenzoic acid (DHBA) concentrations in the microdialysis perfusate was confirmed during both ischemia and reperfusion phase. Although the temporal profile and amount of salicylate hydroxylation were heterogeneous among individual animals, integrated 2,3-DHBA concentrations during reperfusion were correlated positively with integrated glutamate concentrations during ischemia and negatively with mean postischemic CBF. These relationships suggest a possible association of the enhanced production of 2,3-DHBA during reperfusion with larger amounts of intraischemic glutamate release and lower levels of post-ischemic CBF.

Topics: Acid-Base Imbalance; Analysis of Variance; Animals; Cerebral Cortex; Cerebrovascular Circulation; Chromatography, High Pressure Liquid; Free Radical Scavengers; Gentisates; Glutamic Acid; Hydroxybenzoates; Hydroxylation; Iron Chelating Agents; Ischemic Attack, Transient; Laser-Doppler Flowmetry; Male; Rats; Rats, Sprague-Dawley; Regression Analysis; Salicylates; Salicylic Acid

To obtain direct evidence of oxygen radical activity in the course of cerebral ischemia under different intraischemic temperatures, we used a method based on the chemical trapping of hydroxyl radical in the form of the stable adducts 2,3- and 2,5-dihydroxybenzoic acid (DHBA) following salicylate administration. Wistar rats were subjected to 20 min of global forebrain ischemia by two-vessel occlusion plus systemic hypotension (50 mm Hg). Intraischemic striatal temperature was maintained as normothermic (37 degrees C), hypothermic (30 degrees C), or hyperthermic (39 degrees C) but was held at 37 degrees C before and following ischemia. Salicylate was administered either systemically (200 mg/kg, i.p.) or by continuous infusion (5 mM) through a microdialysis probe implanted in the striatum. Striatal extracellular fluid was sampled at regular intervals before, during, and after ischemia, and levels of 2,3- and 2,5-DHBA were assayed by HPLC with electrochemical detection. Following systemic administration of salicylate, stable baseline levels of 2,3- and 2,5-DHBA were observed before ischemia. During 20 min of normothermic ischemia, a 50% reduction in mean levels of both DHBAs was documented, suggesting a baseline level of hydroxyl radical that was diminished during ischemia, presumably owing to oxygen restriction to tissue at that time. During recirculation, 2,3- and 2,5-DHBA levels increased by 2.5- and 2.8-fold, respectively. Levels of 2,3-DHBA remained elevated during 1 h of reperfusion, whereas the increase in 2,5-DHBA persisted for 2 h. The increases in 2,3- and 2,5-DHBA levels observed following hyperthermic ischemia were significantly higher (3.8- and fivefold, respectively). In contrast, no significant changes in DHBA levels were observed following hypothermic ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Body Temperature; Corpus Striatum; Dialysis; Free Radicals; Gentisates; Hydroxybenzoates; Hydroxyl Radical; Ischemic Attack, Transient; Kinetics; Male; Rats; Rats, Wistar; Reperfusion; Salicylates; Salicylic Acid

Transient global ischemia may lead to persistent production of reactive oxygen species in selected brain regions thereby contributing to selective vulnerability to ischemia. Using cerebral microdialysis, we assessed the production of the highly reactive hydroxyl radical (OH.) in rat hippocampus during global ischemia and reperfusion (IR). During IR, perfusate containing salicylic acid was collected and analyzed for non-enzymatic hydroxylation of salicylate to 2,3-DHBA. Since 21-aminosteroids can attenuate excitatory amino acid-mediated OH. production in the brain, we repeated the experiments after administration of the 21-aminosteroid, U-74389G. The data indicate that 2,3-DHBA level increased progressively between 15 and 60 min after reperfusion, reaching values nearly three times the baseline value at 60 min. U-74389G, given 30 min before ischemia, greatly attenuated the increase in 2,3-DHBA during reperfusion. This is the first evidence for prolonged OH. production in the hippocampus after reperfusion in vivo which can be prevented by 21-aminosteroids.

Topics: Animals; Antioxidants; Cerebrovascular Circulation; Hippocampus; Hydroxybenzoates; Hydroxyl Radical; Hydroxylation; Ischemic Attack, Transient; Male; Pregnatrienes; Rats; Rats, Sprague-Dawley; Reactive Oxygen Species; Salicylates; Salicylic Acid

Brain is extremely susceptible to oxidative damage. Utilizing a series of novel approaches, we have demonstrated that oxidative damage occurs during an ischemia/reperfusion insult (IRI) to brain. Thus, we have demonstrated that an IRI to Mongolian gerbil brain results in: (1) an enhanced rate of salicylate hydroxylation, implicating an increased flux of hydroxyl free radicals; (2) an enhanced flux of free radicals as determined by spin-trapping; (3) an enhanced level of endogenous protein oxidation; (4) a decrease in glutamine synthetase (GS) activity, an enzyme very sensitive to oxidative damage; and (5) demonstration of protection from an IRI by administering the spin-trapping agent alpha-phenyl-tert-butyl nitrone (PBN). The novel observation that PBN offers protection from the lethality brought on by a brain IRI appears to be clearly linked to the ability of the administered spin-trap to inhibit oxidative damage as evidenced by the decreased amount of brain protein oxidation and the prevention of an IRI-mediated loss of GS activity in treated animals. Aged gerbils are more sensitive to the lethal action of a brain IRI than younger animals, but they are protected by PBN administration as are the younger animals. Older gerbils have a significantly higher level of oxidized protein in the brain. Older gerbils have decreased activities of GS and neutral protease, the enzyme that removes oxidized protein, than younger animals. Chronic twice daily administration of PBN (32 mg/kg) for 14 days to older animals significantly lowered brain oxidized protein levels and raised GS and neutral protease activity to those observed in younger animals. Cessation of PBN administration resulted in a time-dependent restoration of protein oxidation levels and enzyme activities back to those observed prior to spin-trap administration. Older gerbils exhibit significantly higher errors in a radial arm maze than younger animals, but older gerbils that had received chronic daily treatments of PBN (32 mg/kg) for 14 days committed significantly less errors than untreated controls. The errors committed in PBN-treated animals was decreased down to the level of those observed in younger animals. Clearly the spin-trapping agent, PBN, appears to have promise in: (1) elucidation of the role of oxidative damage in normal brain function during aging, (2) understanding the development of pathological conditions, and (3) development of treatment regimens for prevention of damage that occurs d

Topics: Animals; Brain; Cerebral Cortex; Cyclic N-Oxides; Free Radicals; Gerbillinae; Glutamate-Ammonia Ligase; Ischemic Attack, Transient; Nitrogen Oxides; Oxidation-Reduction; Oxygen; Reperfusion Injury; Salicylates; Salicylic Acid; Spin Labels

Evidence is presented which implicates increased oxygen free radicals during ischemia reperfusion of gerbil brain. Salicylate, which reacts with hydroxyl free radicals to yield dihydroxybenzoic acid (DHBA), was used as an in vivo trap. Brain ischemia for at least 5 min followed by reperfusion yielded significantly increased brain DHBA. Without reperfusion or with only 2 min of ischemia and then reperfusion, the production of DHBA was not increased. Increased levels of DHBA in brain correlated with ischemia reperfusion-mediated behavioral modification of gerbils, but salicylate administration did not protect against the behavior changes.

Topics: Animals; Brain Chemistry; Free Radicals; Gerbillinae; Hydroxybenzoates; Ischemic Attack, Transient; Motor Activity; Oxygen; Salicylates; Salicylic Acid; Time Factors

Topics: Aged; Dipyridamole; Female; Humans; Ischemic Attack, Transient; Isoindoles; Male; Middle Aged; Phenylbutyrates; Platelet Aggregation Inhibitors; Recurrence; Salicylates; Salicylic Acid

The clinical picture of transient global amnesia (TGA) is discussed on the basis of the clinical findings in 19 patients. The central symptom is an acute memory loss, leading to disorientation, helplessness and pseudo-confusion. The symptoms last for several hours and then fade away. Pathogenetically a functional impairment of the limbic system is proposed. Most cases of TGA are due to ischaemic disease; rare causes are epileptic seizures, tumours, encephalitis and toxic or metabolic conditions. In order to clarify the aetiology and initiate appropriate therapy meticulous neurological investigation is necessary. The spontaneous prognosis of ischaemic forms is favourable, whilst in other cases it depends on the primary condition.

Topics: Adult; Amnesia; Brain Ischemia; Carbamazepine; Child; Female; Humans; Ischemic Attack, Transient; Limbic System; Male; Memory, Short-Term; Middle Aged; Platelet Aggregation; Salicylates