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Prevalence of abnormal glucose tolerance following a transient ischemic attack or ischemic stroke.

BACKGROUND: Despite current preventive therapies, patients with transient ischemic attack (TIA) and ischemic stroke remain at high risk for recurrent brain disease and cardiovascular events. In an effort to develop new therapies, abnormal glucose tolerance has recently been proposed as an interventional target. Among persons not otherwise known to be diabetic, impaired glucose tolerance (IGT) and diabetic glucose tolerance (DGT) are each associated with an increased risk for incident vascular disease, vascular disease mortality, and all-cause mortality. We conducted this study to determine if IGT and DGT are sufficiently common among patients with TIA and ischemic stroke to warrant therapeutic trials of antihyperglycemic agents. METHODS: Men and women older than 45 years were recruited from 3 hospitals in south central Connecticut. Eligibility criteria included a recent TIA or nondisabling ischemic stroke, no history of physician-diagnosed diabetes mellitus, and a fasting plasma glucose level less than 126 mg/dL (<7.0 mmol / L). After an overnight fast, subjects were admitted to a clinical research center for a standard 75-g oral glucose tolerance test. Impaired glucose tolerance was defined by a 2-hour plasma glucose value of 140 to 199 mg/dL (7.8-11.0 mmol / L) and DGT by a value of 200 mg/dL or greater (> or =11.1 mmol/L). RESULTS: Between June 2000 and August 2003, we enrolled 98 eligible patients. The average time from TIA or stroke to measurement of glucose tolerance was 105 days (range, 24-180 days) and the median age was 71 years. Twenty-seven subjects (28%) had IGT and 24 (24%) had diabetes. In a forward stepwise logistic regression model, only a fasting plasma glucose level of 110 mg/dL or greater (> or =6.1 mmol / L) and lower waist circumference were associated with an increased risk for IGT or DGT. CONCLUSIONS: Impaired glucose tolerance and DGT are present in most persons with a recent TIA or ischemic stroke who have no history of diabetes and a fasting plasma glucose level less than 126 mg/dL (<7.0 mmol / L). Our findings bring new urgency to the initiation of research to examine the effectiveness of antihyperglycemic therapies among patients with cerebrovascular disease and abnormal glucose tolerance.

Age Distribution↗

Adhesive glycoproteins CD11a and CD18 are upregulated in the leukocytes from patients with ischemic stroke and transient ischemic attacks.

Leukocytes may have an important role in the pathogenesis of brain injury after ischemia. Expression of adhesion molecules on leukocytes and/or endothelia is needed for leukocytes to adhere to endothelia and infiltrate into the injured brain. The purpose of the present pilot study is to delineate whether the expression of leukocyte adhesion molecules, CD11a and CD18, are upregulated in patients with ischemic stroke and transient ischemic attack. Ten patients with ischemic stroke, 6 with transient ischemic attack (TIA), and 11 age and risk factor matched controls were studied. Using immunofluorescence phenotyping and flow cytometry, leukocyte membrane expression of CD11a and CD18 were measured within 72 h after onset of ischemia. Follow-up measurements were performed at 5-7 days after ictus in 6 patients with stroke, and at 3-5 days after ictus in 3 patients with TIA. CD11a immunofluorescence (IF) was significantly increased within 72 h after onset of symptoms in patients with stroke as well as TIA compared with the control group (p < 0.017). IF of CD18 also increased in both patient groups, but significance was reached only in the TIA group (p < 0.05). No difference of CD11a and CD18 IF was detected between stroke and TIA groups. Follow-up measurement of CD11a and CD18 showed a trend of decrease, but CD11a IF remained significantly elevated compared with the control group (p < 0.017). Expression of leukocyte adhesion molecules CD11a, and CD18 are upregulated in patients with ischemic stroke and TIA. Although these data are preliminary, our data suggest that these molecules are associated with cerebrovascular disorders including ischemic stroke and TIA.

Aged↗

[Comparative study of nicardipine versus placebo in the prevention of cognitive deterioration in patients with transient ischemic attack].

The neuropsychological follow up of transient ischemic attacks can provide a model for evaluating the efficiency of a drug in vascular dementia. A double blind study has been conducted using nicardipine, a calcium-antagonist, as opposed to a placebo in 40 patients with transient ischemic attacks, over a six month period. The patients were evaluated according to a Wechsler's intelligence scale, and their memory was also tested before and after this period. Although no alterations were registered on either scale, some differences did appear in certain sub-tests, especially as regards the verbal coefficient. This pilot study has provided information concerning the possible beneficial effect of the drug, which should be proven by means of a larger-scale study.

Aged↗

Effects of an individualized multimedia computer program for health education in patients with a recent minor stroke or transient ischemic attack - a randomized controlled trial.

BACKGROUND: Transient ischemic attack (TIA) and stroke patients often show a striking lack of knowledge about their disease. We developed a computer program that provided health education fitting the educational level, risk profile and symptoms of patients and evaluated it in a randomized controlled trial. METHODS: Transient ischemic attack or minor stroke patients were allocated to health education by a physician (n = 32) or to a combination of education by a physician and the computer program (n = 33). Knowledge was tested by means of a questionnaire at 1 and 12 weeks after inclusion. The maximum possible score was 71 points. RESULTS: Overall knowledge was low - the mean score was 43.6 at 1 week and 42.0 points at 12 weeks for both the groups. The intervention group had slightly better scores at 1 week after using the computer program, 45.4 vs 41.5 (P = 0.09), with the difference increasing to 4.3 points after (post-hoc) adjustment for age and level of education (P = 0.06). After 12 weeks, the score in the intervention group dropped significantly to 42.0 points (P = 0.05), and was no longer different from the standard group. CONCLUSION: This study did not show a lasting effect of health education by an individualized computer program on the knowledge of TIA and minor stroke patients.

Aged↗

Positive platelet scintigram of a vertebral aneurysm presenting thromboembolic transient ischemic attacks.

We describe a patient with transient ischemic attacks secondary to a giant aneurysm who showed increased activity on platelet scintigrams at the origin of the left vertebral artery. This is assumed to be the first report of a presumed embolizing aneurysm with positive activity of labeled platelets. Platelet scintigraphy is useful for diagnosing transient ischemic attacks as being secondary to an aneurysm and was proved to provide direct evidence of a thromboembolic source in vivo.

Adult↗

Cerebral infarction verified by cranial computed tomography and prognosis for survival following transient ischemic attack.

Of 564 consecutive patients with transient ischemic attack, 350 (62%) had cranial computed tomography performed. Except for date of admission and smoking history, there were few differences between the patients evaluated with computed tomography and the 214 who were not. Cerebral infarcts were found in 59 (17%) of the 350 tomographic evaluations. Previous clinically diagnosed stroke, older age, and male sex were all significantly associated with the occurrence of tomographically verified infarcts (p less than 0.05). After controlling for stroke history and other important covariates, patients with tomographically verified infarcts had significantly shorter survival times than did patients without evidence of infarction on computed tomography (p = 0.035). Thus, cranial computed tomography findings appear to have important prognostic value for estimating survival following transient ischemic attack.

Cerebral Angiography↗

Midazolam challenge reinduces neurological deficits after transient ischemic attack.

BACKGROUND AND PURPOSE: A transient ischemic attack (TIA) in the brain is classically considered a syndrome lasting <24 hours. Having previously shown that an experimental challenge with the GABAA agonist midazolam in recovered stroke patients can reinduce the acute clinical state, we determined whether TIA patients would demonstrate a similar effect. METHODS: Four right-handed patients participated: 3 with clinical TIA presumed to have affected the left hemisphere within the previous 24 to 72 hours and no evidence of a new lesion on diffusion-weighted and fluid-attenuated inversion recovery imaging, and 1 patient with an asymptomatic temporal arteriovenous malformation. The TIA duration ranged from 30 minutes to 3 hours. Each patient underwent baseline testing for motor function and aphasia, after which intravenous midazolam was delivered until mild drowsiness was detected. Patients were tested during the peak drug effect and again after 2 hours when sedation had dissipated. RESULTS: No patient showed weakness or aphasia at baseline. After administration of midazolam, all 3 TIA patients demonstrated re-emergence of features that characterized their recent transient neurological syndromes (right-sided weakness and/or aphasia) but no left-sided findings. The arteriovenous malformation patient who had never been symptomatic showed no drug effect. Two hours later, all TIA patients returned to their normal clinical state. CONCLUSIONS: Patients who had suffered recent transient cerebral ischemic episodes and were neurologically intact with negative diffusion-weighted imaging showed re-emergence of prior focal deficits after administration of a benzodiazepine in a dose that produces light sedation. These findings suggest that presumed TIA may produce neuronal dysfunction beyond the symptomatic period.

Adult↗

Cerebral infarct in apparent transient ischemic attack.

Fifty-seven patients with transient ischemic attacks in the carotid territory had CTs 3 to 28 days after the last episode. Sixteen (28%) showed an infarct appropriate to the symptoms. Infarcts were more likely with longer mean duration of attacks, longer duration of the longest attack, longer total duration of symptoms, and smaller number of attacks. Age, sex, type and extent of hemisphere symptoms, and vascular risk factors had no influence. If attacks lasted more than 45 to 60 minutes, the risk of infarction was more than 80%; most were actually infarcts. So-called TIAs included two subgroups, true TIA and CITS (cerebral infarction with transient signs), which corresponded respectively to a short (mean, 21 minutes) or long (mean, 6 hours) duration of attack.

Aged↗

Incidence trends of ischemic stroke and transient ischemic attacks in a well-defined French population from 1985 through 1994.

BACKGROUND AND PURPOSE: The changing incidence of ischemic stroke is of major concern in view of its public health impact, to define the population concerned, to identify risk factors, and to set up health-care systems. The aim of this study was to evaluate the time trends associated with the incidence of all the subtypes of ischemic stroke and transient ischemic attacks in a well-defined population for 10 years. METHODS: Since 1985, a population registry has recorded each patient living in Dijon (France) who suffered from a cerebrovascular disease (CVD) regardless of the type of management. This study involved all patients suffering from their first ischemic stroke and their first transient ischemic attacks (TIAs) during 1 calendar year between January 1, 1985 and December 31, 1994. The incidence changes according to age, sex, and type of cerebral ischemic event (cortico-subcortical infarct, lacunar infarct, and TIA) were studied on the basis of their annual variations. RESULTS: During the 10-year study period, 834 cortico-subcortical infarcts (52.1%), 296 lacunar infarcts (18.5%), 369 TIAs (23.1%), and 101 undetermined ischemic strokes (6.3%) were collected. The incidence of all ischemic events was relatively stable in both sexes over the 10-year period. However, the incidence rates differed according to age and type of ischemia. An increased incidence of cerebral cortico-subcortical infarct was observed in patients older than 75 years of age (+5.45% annual change [AC] in men, P<0.05; +5. 09% AC in women, NS). In parallel, a higher proportion of emboligenic cardiac arrhythmias was observed in these patients (P<0. 001). The incidence of lacunar infarcts tended to decrease, regardless of age but mainly in men under younger than 75 years of age (-12.74% AC in men, NS; +0.31% AC in women, NS). The incidence of TIAs was relatively stable in both sexes. Because our population consisted of a large number of elderly subjects, the increase in cardioembolic causes could partially explain the increased incidence of cerebral cortico-subcortical infarcts in patients older than 75 years of age. CONCLUSIONS: These preliminary data emphasize the importance of stroke surveillance in considering the variations of the different mechanisms of ischemic cerebrovascular disease. Although the incidence of TIA is stable and the incidence of lacunes tends to decrease in men, mainly before 75 years of age, we emphasize the rise of the crude incidence of cortico-subcortical infarcts in men older than 75 years of age, induced by an increase in cardioembolic causes.

Age Factors↗

Transient ischemic attack: the presenting manifestation of transient asystole.

A patient with a focal transient neurologic deficit and no evidence of other underlying disease as an etiology is diagnosed with episodic asystole. His neurologic deficit was reproduced with episodes of asystole. The combination of asystole and localized intracranial atherosclerotic disease can produce focal neurologic deficits and should be considered in the differential for transient ischemic attack. It is easily preventable and responds to permanent implantation of a transvenous pacemaker.

Aged↗

Headache associated with transient ischemic attacks.

Sixty (29%) of 205 consecutive patients with transient ischemic attacks registered in a hospital stroke data base had headache within 72 hours of onset. Headache was significantly more common in nonsmokers (odds ratio = 2.8; 95% confidence interval = 6.7 to 1.2). Headache was infrequent in patients with amaurosis fugax, and was not significantly associated with any other particular clinical presentation of transient ischemic attack. Headache was more common in vertebrobasilar (33%) than in carotid distribution (24%) episodes, and was not rare in transient ischemic attacks presenting as lacunar syndromes (29%). Headache was less frequent in patients whose computerized tomograms showed an infarct appropriate to the symptoms (odds ratio = 0.2; 95% confidence interval = 0.02 to 1.4). A diffuse headache was more common in patients with lacunar events than in patients with cortical attacks (odds ratio = 3.0; 95% confidence interval = 13 to 0.07). No other association was found between headache location and the presumed involved vascular territory. Headache in patients with transient ischemic attacks is poorly related/explained by the clinical characteristics of the ischemic event.

Aged↗

Short-term outcome of medically treated patients with transient ischemic attacks, reversible ischemic neurologic deficits and strokes with minimum residuum.

62 patients with transient ischemic attack (TIA), 60 with reversible ischemic neurologic deficit (RIND) and 57 with stroke with minimum residuum (SMR) were followed, in a retrospective survey, from the first 7 days to the 3rd month of evolution. 90 received anticoagulant treatment, 66 antiplatelet treatment and 23 other or no treatment. 5 patients developed strokes with moderate or severe disability; no patient suffered a myocardial infarction or died. No influence of the type of treatment or of the clinical group (TIA, RIND and SMR) on the follow-up complications could be detected. There seems to be a group with a greater risk of developing further cerebral infarction, which is characterized by the occurrence of multiple TIAs for several days before the event.

Anticoagulants↗

Cerebral revascularization for transient ischemic attacks.

Thirty-one patients with cerebral transient ischemic, attacks and ipsilateral internal carotid artery occlusion without contralateral internal carotid artery occlusion or stenosis were treated with a surgical anastomosis between a superficial temporal artery and a cortical branch of the middle cerebral artery of the symptomatic hemisphere. The anastomosis was successful in 28 patients. Recurrent transient ischemic attacks were abolished in 23 patients and reduced in three. Two patients, one with a patent anastomosis, had strokes during the follow-up period. Of seven patients who refused the operation, two had strokes, two noted a reduction of transient ischemic attacks, two noted no change, and one became asymptomatic.

Adult↗

Relevance of transient ischemic attack to early neurological recovery after nonlacunar ischemic stroke.

BACKGROUND: We hypothesized that previous transient ischemic attack (TIA) had a favorable effect on early outcome after acute nonlacunar ischemic stroke. METHODS: Data of 1,753 consecutive patients with ischemic stroke collected from a prospective hospital-based stroke registry were studied. A comparison was made of the groups with and without previous TIA. Favorable outcome included spontaneous neurological recovery or grades 0-2 of the modified Rankin scale at hospital discharge. RESULTS: Previous TIA occurred in 55 (11.5%) of 484 patients with lacunar stroke and in 166 (13.1%) of 1,269 patients with nonlacunar stroke. The percentage of nonlacunar ischemic stroke patients with favorable outcome was 21.7% in those with a history of TIA compared to 15% without TIA (p < 0.03). In the lacunar stroke group, differences were not significant. In the multivariate analysis, TIA was an independent predictor of spontaneous in-hospital recovery. CONCLUSIONS: Prior TIA was associated with a favorable outcome in nonlacunar ischemic stroke, suggesting a neuroprotective effect of TIA possibly by inducing a phenomenon of ischemic tolerance allowing better recovery from a subsequent ischemic stroke.

Activities of Daily Living↗

Cerebral amyloid angiopathy presenting as transient ischemic attacks. Case report.

Cerebral amyloid angiography can cause ischemic stroke and transient ischemic attacks (TIA's), as illustrated by this case report and literature review. It is possible that the use of anticoagulant or platelet-antiaggregant drugs in elderly patients with TIA's but no angiographic abnormalities may increase the risk of hemorrhage from unsuspected amyloid angiopathy.

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[Comparison of vascular risk factors profiles for transient ischemic attacks and ischemic stroke].

BACKGROUND AND OBJECTIVE: To determine vascular risk factor (VRF) profiles in transient ischemic attack (TIA) and ischemic stroke. PATIENTS AND METHOD: We studied 239 patients with TIA and 1,473 ischemic stroke patients included in a prospective stroke registry over a 10-year period. RESULTS: Main VRF were: hypertension, hyperlipidemia, diabetes mellitus and atrial fibrillation. In the multivariate analysis, prior ischemic stroke (OR=1.65; 95% CI, 1.07-2.56), atrial fibrillation (OR=1.60; 95% CI, 1.14-2.26) and current use of warfarin treatment (OR=0.34; 95% CI, 0.13-0.94) were the only independent risk factors associated with ischemic stroke. CONCLUSIONS: Different potentially modifiable vascular risk factor profiles were identified in ischemic stroke versus TIA. This suggests that there are pathogenic differences between TIA and ischemic strokes.

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Transient ischemic attack: a neurologic emergency.

Classically, a transient ischemic attack (TIA) has been defined as an acute episode of neurologic symptoms lasting less than 24 hours attributed to focal ischemia in a vascular distribution of the brain or retina. Stroke and TIA share similar risk factors, evaluation, and secondary prevention. However, evaluation of patients with TIA has traditionally lacked the same urgency that has been directed to acute stroke, probably because patients with TIA are at baseline neurologically when the diagnosis is made. Recently, several studies have found a high risk of stroke shortly after TIA. Furthermore, recent evidence suggests that early recovery from ischemia actually is associated with greater instability. Identifying patients with the highest risk of recurrent ischemic events for urgent evaluation and intervention is key in secondary stroke prevention. This article reviews the current literature on new concepts about TIA, subsequent risk of stroke, and guidelines on evaluation and treatment.

Emergency Service, Hospital↗

[The transient ischemic attack, between diagnosis and treatment].

The transient ischemic attack (TIA) in cerebral circulation in 161 patients is studied. The causes and favouring factors are analysed, arterial hypertension and dyslipidemias representing 70% of the factors that might be incriminated in the physiopathology of TIAs. The paraclinical and therapeutic results demonstrate that in over 30% of the cases the etiology could be explained by "the multiple defect theory", the importance of transcranial Doppler in the diagnosis and prognosis of TIA, especially in the young patients, being underlined.

Age Distribution↗