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Results for “Transient ischemic attack”

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PubMed1990

Perfusion insufficiency in limb-shaking transient ischemic attacks.

We describe a 63-year-old man with severe bilateral internal carotid artery disease who presented with repeated, brief attacks of left limb shaking precipitated by his standing up. Cerebral blood flow measured by xenon-133 inhalation showed reduced resting flows and a focal perfusion deficit in the right dorsofrontal and upper rolandic regions. Blood flow velocity and pulsatility index of the right middle cerebral artery measured by transcranial Doppler ultrasonography were also reduced. With hypercapnic challenge, both hemispheric tissue perfusion and blood flow velocity showed impaired reactivity. With induced hypotension, the focal perfusion deficit in the right dorsofrontal region was accentuated. Following right internal carotid endartectomy, resting cerebral blood flow and blood flow velocity improved, as did hypercapnic vasoreactivity. These reversible deficits in cerebral blood flow and vasoregulation, which were maximal in the dorsofrontal region, are consistent with low perfusion in the border zone territory or the distal fields and demonstrate that hemodynamic failure is the likely mechanism for limb-shaking transient ischemic attacks from severe carotid artery disease.

Biomechanical Phenomena↗

PubMed1991

An unusual cause of transient ischemic attacks: case report.

A 42-year-old black man, a physician, presented with a three week history of intermittent right arm and leg numbness and weakness, lasting about five minutes. This was not associated with headache, visual changes, seizures, aphasia or loss of consciousness. There was no history of head trauma, migraines, or previous attacks. Positive findings on physical examination were confined to a blood pressure of 182/80; evidence of hypertensive retinopathy; normal carotid pulses without bruits; and a Grade II/VI systolic ejection murmur with normal sinus rhythm. Initial hematocrit was 25.7%; white blood cell count 14,000 cu/mm with a normal differential; platelet count 532,000 cu/mm. An electrocardiogram showed left ventricular hypertrophy. Duplex scan demonstrated normal carotid bifurcations bilaterally, and arteriogram revealed no carotid or intracranial pathology. Hemoglobin electrophoresis revealed sickle cell disease of the SS type. He was treated with transfusion therapy and has remained asymptomatic at 40 months. Approximately 20% of children with the SS type sickle cell disease will have cerebrovascular symptoms caused by small intracranial artery occlusion due to sludging of the abnormal hemoglobin. This unusual cause of transient ischemic attacks can occur in older patients of African-American ancestry and must be recognized to enable early and effective therapy with exchange transfusion.

Adult↗

PubMed2003

Association of parental history of stroke with clinical parameters in patients with ischemic stroke or transient ischemic attack.

BACKGROUND AND PURPOSE: Data regarding hereditary influences on stroke remain controversial. We investigated possible associations of a family history of stroke with clinical parameters in a large cohort of well-documented patients with ischemic cerebrovascular events, with special reference to sex-specific differences. METHODS: We analyzed the association between a maternal and/or paternal history of stroke and clinical parameters in 1564 patients with known maternal and paternal history of stroke and suffering from ischemic stroke or transient ischemic attack within the Vienna Stroke Registry. RESULTS: Patients with a maternal history of stroke were significantly more often female (54%) than those without (44%; P=0.003). Hypertension was more prevalent in female patients with than in those without a maternal history of stroke (87% versus 74%; P=0.001). These associations remained significant after multivariate adjustment (adjusted odds ratio, 1.9; 95% CI, 1.1 to 3.5; P=0.024). Of those female patients with an echocardiogram (n=225), those with a maternal history of stroke more often had left ventricular hypertrophy (48%) than those without (20%) (adjusted odds ratio, 3.6; 95% CI, 1.5 to 8.2; P=0.003). In contrast, hypertension was equally prevalent in male patients with or without a maternal history of stroke (75% versus 74%; P=0.754). We found no significant associations of clinical parameters with a paternal history of stroke. CONCLUSIONS: Our results indicate a sex-specific relationship between a maternal history of stroke and the prevalence of hypertension and left ventricular hypertrophy in female patients with ischemic cerebrovascular events.

Aged↗

PubMed2005

Family history of stroke does not predict risk of stroke after transient ischemic attack.

BACKGROUND AND PURPOSE: Animal models suggest a genetic contribution to cerebral susceptibility to ischemia. Family history of stroke (FHxstroke) is a risk factor for ischemic stroke, but there is significant confounding by heritability of hypertension and other intermediate phenotypes, and it is uncertain whether genetic factors have a direct independent influence on cerebral susceptibility to ischemia in man. METHODS: We related detailed FHxstroke to baseline characteristics and subsequent risk of stroke in 2 population-based incidence studies and a consecutive hospital-referred series of patients with recent transient ischemic attack (TIA). RESULTS: In none of the cohorts or the pooled data (757 patients; 5515 patient years follow-up; 200 ischemic strokes; 126 myocardial infarctions [MIs]) did FHxstroke predict ischemic stroke (odds ratio [OR], 0.87; 95% CI, 0.57 to 1.32). No associations were revealed by analyses stratified by age or hypertension in the proband, FHx(stroke) in parents versus siblings, number of affected relatives, or their age at stroke. FHxstroke was unrelated to presence of ischemic lesions on baseline computed tomography (OR, 0.96; 0.52 to 1.76) or risk of MI during follow-up. There was no bias attributable to any relationship between FHxstroke and risk factor control or medication. CONCLUSIONS: Family history of stroke does not predict risk of ischemic stroke after TIA.

Aged↗

PubMed2003

Determination of lipid profiles and use of statins in patients with ischemic stroke or transient ischemic attack.

BACKGROUND AND PURPOSE: Statins reduce the risk of myocardial infarction and stroke in patients with vascular disease. Inappropriate serum lipid determination and underuse of statins have been documented in patients with coronary artery disease. Evaluation of hyperlipidemia and treatment with statins in patients with recent ischemic cerebrovascular events have not yet been investigated. METHODS: We determined the frequency of total cholesterol (TC) and low-density lipoprotein cholesterol measurements and the use of statins in a multicenter prospective cohort study of 1743 patients with acute ischemic stroke or transient ischemic attack (TIA). Using multivariate logistic regression analysis, we determined the influence of several clinical variables on lipid measurements and the prescription of statins at hospital discharge. RESULTS: TC was measured in 90% and low-density lipoprotein cholesterol was measured in 48% of the patients. Differences between the centers accounted for most of the observed variability in a multivariate model. Statin prescription also varied widely between the centers. The prescription of a statin at discharge was most strongly associated with statin intake before the event and with increasing TC levels; elderly patients received statins less often. Coronary artery disease, peripheral artery disease, and other manifestations of atherosclerosis were not independently associated with the use of statins; 68% of the patients with manifest atherosclerosis and TC levels >200 mg/dL were discharged without a statin. CONCLUSIONS: The determination of serum lipid profiles varies widely between different centers. Statins are highly underused in patients with recent ischemic stroke or TIA, particularly in those in whom statins are indicated according to existing recommendations (eg, patients with additional coronary artery disease and hypercholesterolemia). Currently, international guidelines concerning the use of statins are not adequately implemented in clinical practice in patients with stroke or TIA.

Aged↗

PubMed2003

Delayed transient ischemic attacks kill some CA1 neurons previously salvaged with postischemic hypothermia: neuroprotection undone.

Delayed hypothermia reduces ischemic hippocampal CA1 injury. However, there are residual structural and functional abnormalities. Therefore, we studied whether these apparently vulnerable rescued neurons are susceptible to secondary insults. All gerbils were subjected to normothermic forebrain ischemia (ISC, 5 min) or SHAM operation. Gerbils were treated with mild hypothermia (HYPO; 33 degrees C for 24 h+35 degrees C for 24 h) beginning 12 h after surgery, or they remained normothermic (NORMO). Then 5 and 6 days following ISC/SHAM operation gerbils received sublethal transient ischemic attacks (TIA, 1.5 min) or sham (SH) surgeries. Behavioral testing was done and animals survived for 30 days for quantification of medial, middle and lateral CA1 sector cell death. The SHAM groups were not significantly different. The ISC+NORMO+SH group lost 87.3% (of SHAM) of medial CA1 neurons, which was not significantly exacerbated in the ISC+NORMO+TIA group (91.1%, P=0.633). However, the ISC+HYPO+TIA group (58.8% loss) had significantly more cell death than the ISC+HYPO+SH group (42.8%; P=0.035), although CA1 protection was still better than in ISC+NORMO groups (P<0.001). Trends were similar in middle and lateral CA1, but the deleterious effects of TIAs were not statistically significant. Behavioral testing did not distinguish groups with or without TIA, but did reveal deficits in ISC+NORMO groups and protection in ISC+HYPO groups. These data, like previous ultrastructural findings, show that while most hypothermia-rescued CA1 neurons are healthy, some are susceptible. Perhaps other neuroprotectants, especially weaker ones, might be undone by delayed insults (e.g. TIA, fever).

Animals↗

PubMed2002

Recurrent transient ischemic attacks as the initial presenting manifestation of type A aortic dissection.

A case is reported of an 84-year-old woman with recurrent episodes of aphasia and right-sided weakness with spontaneous complete resolution associated with hypotension. She subsequently developed lower gastrointestinal bleeding, ischemic toes, and anuria without associated chest pain. An emergent transesophageal echocardiography showed a type A aortic dissection with aortic valve insufficiency and tamponade. Emergent thoracotomy was performed, which confirmed a severe acute type A aortic dissection. This is a reported case of acute painless aortic dissection presenting initially as recurrent transient ischemic attacks. The etiology of focal neurologic deficits should be crucially determined by an experienced clinician prior to thrombolytic administration. This case illustrates the importance of aortic disease in the etiology of acute stroke syndromes.

Aged↗

PubMed1988

Carotid body tumor: unusual cause of transient ischemic attacks.

Carotid body tumors are an unusual cause of transient ischemic attacks. The cases reported in the literature have been limited to the postoperative period. We report a patient with bilateral carotid body tumors and transient ischemic attacks as the presenting syndrome. A low-perfusion state could explain his symptomatology.

Carotid Body Tumor↗

PubMed2005

Screening for aspirin responsiveness after transient ischemic attack and stroke: comparison of 2 point-of-care platelet function tests with optical aggregometry.

BACKGROUND AND PURPOSE: Recent studies suggest that patients who do not respond to aspirin (ASA) therapy may be at increased risk of ischemic vascular events. The availability of simple to use point-of-care (POC) platelet function tests now potentially allows aspirin nonresponsiveness to be identified in routine clinical practice. However, there are very few data on whether the different tests produce consistent results. We therefore compared 2 POC tests (PFA-100 device and the Ultegra-RPFA [RPFA]) with conventional light transmission aggregometry (LTA). METHODS: Platelet function was assessed by all 3 tests in 100 patients receiving low-dose ASA therapy after transient ischemic attack (TIA) or ischemic stroke. RESULTS: The incidence of ASA nonresponsiveness was 17% by the RPFA and 22% by the PFA-100, compared with only 5% by LTA (ie, as defined with both arachidonic acid and ADP). Agreement between the RPFA and the PFA-100 and arachidonic acid induced LTA was poor (kappa=0.16, 95% CI, -0.08 to 0.39, P=0.11; and kappa=0.09 -0.12 to 0.30, P=0.32, respectively). Agreement between the 2 POC tests was also poor (kappa=0.14, -0.08 to 0.36, P=0.15). Only 2% of patients were aspirin nonresponders by all 3 tests. CONCLUSIONS: The prevalence of apparent ASA nonresponsiveness was higher with both the POC tests than with LTA. However, agreement between the tests was poor and very few patients were ASA nonresponsive by all 3 tests. Aspirin nonresponsiveness is therefore highly test-specific and large prospective studies will be required to determine the prognostic value of each of the separate tests.

Adult↗

PubMed2005

Carotid atherosclerotic plaques in patients with transient ischemic attacks and stroke have unstable characteristics compared with plaques in asymptomatic and amaurosis fugax patients.

INTRODUCTION: Atherosclerotic carotid artery disease is responsible for a variety of clinical presentations, ranging from asymptomatic to cerebral ischemic events. Considering the upcoming use of noninvasive imaging modalities, plaque characteristics could serve as a marker in the selection of patients eligible for carotid endarterectomy (CEA). This would be more likely if characteristics corresponded with clinical manifestations and were predictive of future events. In this study, we hypothesized that plaque characteristics correlate with the clinical presentation of carotid artery disease. METHODS: We included 404 patients undergoing a carotid endarterectomy (CEA). Ipsilateral clinical symptoms and duplex measurements were recorded. Patients could be asymptomatic (23.5%) or symptomatic with stroke (26.5%), transient ischemic attack (TIA) (36.1%), or amaurosis fugax (AFX) (13.9%). Plaques were stained and semi-quantitatively analyzed for the presence of macrophages, smooth muscle cells, collagen, calcifications, and thrombus. Plaques were categorized in three phenotypes by their overall presentation and the amount of fat. In addition, plaque matrix metalloproteinase (MMP) activity and cytokines expressions were measured. RESULTS: Fibrous, fibro-atheromatous, and atheromatous plaques were observed in 30.2%, 35.6%, and 34.2%, respectively. Atheromatous plaques were more prevalent in patients with stroke and TIA compared with asymptomatic patients or patients with AFX (P = .001). Collagen staining was less evident in patients with TIA and stroke compared with asymptomatic patients or patients with AFX (P < .001). Plaques of patients with TIA and stroke showed significantly higher activity levels of MMP-8 and MMP-9 and higher levels of interleukin-8 compared with asymptomatic and AFX patients. CONCLUSION: Plaque phenotype of patients with TIA is comparable to that of patients with stroke; whereas, the plaque phenotype of patients with AFX resembles the plaque phenotype of asymptomatic patients. Follow-up studies should be encouraged to determine whether plaque characteristics visualized by imaging techniques might help to identify patients most likely to benefit from CEA.

Aged↗

PubMed2004

Fasting plasma glucose and risk of incident ischemic stroke or transient ischemic attacks: a prospective cohort study.

BACKGROUND AND PURPOSE: Diabetes and impaired fasting glucose are diagnosed based on an elevated plasma glucose level after an overnight fast. The diagnostic cutpoint of diabetes arises from the threshold for development of microvascular complications. Our aim was to examine the associations between clinical relevant categories of fasting glucose levels and the risk of incident ischemic stroke. METHODS: Patients with documented coronary heart disease who were screened for inclusion in a secondary prevention clinical trial (n=13,999) were followed-up. At baseline, medical histories were obtained and plasma glucose and lipids assessed at a central study laboratory. During a 6- to 8-year follow-up period 1037 cases were identified with ischemic cerebrovascular disease, of which, after reviewing hospital records with diagnoses of cerebrovascular disease, 576 cases were verified to have had ischemic stroke or transient ischemic attacks. RESULTS: Increasing fasting glucose level categories were positively associated with increasing age, male gender, body mass index, hypertension, total cholesterol, and triglycerides, and were inversely associated with high-density lipoprotein cholesterol and percent high-density lipoprotein of total cholesterol. In comparison with patients with fasting glucose levels of 90 to 99 mg/dL (n=3706) who constitute the largest category, the odds ratios of ischemic cerebrovascular disease, adjusting for potential confounders, were 1.47 (95% CI, 1.07 to 2.02) for fasting glucose <80, 1.22 (0.98 to 1.52) for 80 to 89, 1.27 (1.02 to 1.60) for 100 to 109, 1.60 (1.26 to 2.03) for 110 to 125, 1.82 (1.33 to 2.49) for 126 to 140, and 2.82 (2.32 to 3.43) for >140 mg/dL. Similar J-shaped associations were observed in analysis excluding patients with known diagnosis of diabetes mellitus. CONCLUSIONS: The association between fasting plasma glucose and incident ischemic cerebrovascular events in patients with pre-existing atherothrombotic disease is J-shaped. Rates increase for fasting plasma glucose levels >100 mg/dL and also for those with low fasting glucose levels. These findings may carry important implications for prevention strategies.

Aged↗

PubMed1999

Dominant frequency uncertainty analysis of EEG alpha activity in pilots with transient ischemic attacks.

Objective. To study the characteristics of EEG after transient ischemic attack and to offer reference for screening procedure of aircrew and astronaut selection. Method. The dominant frequency uncertainty of alpha band EEG in 12 pilots (males; age 30 +/- 5) with transient ischemic episodes in middle cerebral artery (MCA) territories and in 20 normal healthy pilots was analyzed with frequency-fluctuation analysis. Result. The dominant probability of the main frequency coinciding with sites affected by transient ischemic attack (TIA) in patient pilots was higher than that in healthy pilots (P<0.01), and the dominant probability ratio logarithmic index I >or= 0 in all patient pilots with normal EEG, but I<0 in all healthy pilots. It was also found that not only I >or= 0, but the second component shifted to lower frequency (8 Hz) in patients with slight focal EEG alterations, i.e. slowing of frequency. The relative entropy values (percentage) were decreased significantly in pilots with TIA as compared with healthy pilots (P<0.05). Conclusion. The dominant frequency uncertainty analysis of alpha band showed clear superiority of computerized evaluation over routine visual assessment for the diagnosis of minor cerebral ischemia. It offers not only a possibility of studying pathophysiological functional parameter, but also the reference for screening procedure in aircrew and astronaut selection.

Acceleration↗

PubMedDate not supplied

Cohort study of exposure to environmental tobacco smoke and risk of first ischemic stroke and transient ischemic attack.

The independent effect of exposure to environmental tobacco smoke (ETS; passive smoking) on the risk of stroke is not well established. We performed a cohort study among 27,698 lifelong nonsmokers with no prior history of stroke, 62% women, aged 30-85 years at enrollment (1979-1985). Self-reported ETS exposure at home and outside home (in hours/week) and stroke risk factors were collected at a health plan in San Francisco and Oakland. Follow-up for hospitalization and death was available through the end of 2000 (median = 16 years). In multivariate analysis adjusting for age, race/ethnicity, educational attainment, marital status, hypertension, diabetes and serum total cholesterol, ETS exposure at home of 20 h or more/week (in relation to <1 h/week) was associated with a 1.29-fold (95% CI 0.75-2.20) and a 1.50-fold (95% CI 1.07-2.09) increased risk of first ischemic stroke among men and women, respectively. No significant associations were found between ETS exposure outside home and ischemic stroke or between exposure to ETS at home or out of home and the risk of transient ischemic attack. Although potentially important confounders (such as dietary habits) were not included in the analysis, high-level ETS exposure at home was independently associated with increased risk of first ischemic stroke among never-smoking women.

Adult↗

PubMed2004

Transient ischemic attack: review for the emergency physician.

In the past few years, the approach to patients with transient ischemic attacks has undergone a transformation. To care for these patients, emergency physicians must understand these changes. They must be comfortable with the diagnosis and treatment of transient ischemic attacks in their emergency department. To this end, we ask and answer the following 6 important questions in this up-to-date review of transient ischemic attacks: (1) How is a transient ischemic attack defined? (2) Does this patient have a transient ischemic attack? (3) Once diagnosed, what diagnostic evaluation should be done (and when)? (4) What treatment should be instituted (and when)? (5) What is the correct disposition? and (6) What are the current medical guidelines?

Anticoagulants↗

PubMed1988

Intraluminal thrombus in the cerebral circulation. Implications for surgical management.

Thrombi defined as intraluminal filling defects detected by angiography were identified in 30 patients (29 in the carotid system, one in the vertebral artery). Stroke was the presentation ipsilateral to the thrombus in 22 patients (12 had previous transient ischemic attacks), transient ischemic attacks occurred alone in seven cases, and one patient was asymptomatic. Angiography revealed a severe stenosis in association with the thrombus in 23 patients, a moderate stenosis in four patients, and, in the three patients with only minimal stenosis presumably due to atherosclerosis, there was evidence for a coagulopathy. Sixteen of the 30 patients were operated on urgently, 10 within 24 hours of detection of the thrombus. Twelve of these 16 surgical patients were given anticoagulation before surgery. At endarterectomy, thrombus was identified in 11 of the 14 surgical patients in whom the thrombus was accessible; the other two surgical patients had intracranial thrombus only. In this group, four of 11 surgical patients with accessible thrombi suffered perioperative episodes of new or larger infarction. Fourteen of the 30 patients initially received medical management with no complication. Eight of these 14 medical patients had repeat angiography; seven exhibited complete resolution of thrombus, and six of these seven patients subsequently underwent delayed endarterectomy for the stenosis. No thrombus was identified at surgery in any of the six. One of the six delayed surgery patients suffered a perioperative stroke. Although these numbers are small, reflecting the rarity of thrombus demonstrated by angiography, undetected thrombus is often found at endarterectomy. Its presence may increase operative risk.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed2005

Does patent foramen ovale promote cryptogenic stroke and migraine headache?

Cryptogenic stroke is a diagnosis of exclusion. These are strokes that occur in people who are usually less than 55 years old, without an identifiable cause. Our sensitivity to these events has been heightened because of the new definitions of a transient ischemic attack. Transient ischemic attack (TIA) is a clinical diagnosis of a neurologic deficit without MRI abnormalities: if there is an MRI abnormality, whether or not that person is symptomatic, it is now defined as a stroke. With these new definitions, and the sensitivity of MRI, we are seeing more cryptogenic strokes. It has been hypothesized that many cryptogenic strokes are caused by small emboli that travel from the legs to the right atrium; during straining (such as a Valsalva maneuver) these emboli can go across a PFO into the left atrium and then travel to the brain, producing a stroke. The problem is that these are very small emboli, approximately 1 to 3 mm, and we can't actually show these small emboli crossing from right to left. However, large emboli have been observed by echocardiography to be trapped in the PFO. So the diagnosis of cryptogenic stroke is a diagnosis of exclusion that is impossible to verify. What is the scope of the problem? Of the 700,000 strokes per year in the United States, 80% of them are ischemic, and 20% of those are defined as cryptogenic. The prevalence of PFO among this cryptogenic stroke population is about 40% to 50%; in the general population, it's only about 20%. Current estimates are that somewhere between 30,000 and 60,000 strokes per year in the U.S. are caused by paradoxical embolism through a PFO. There are some other fascinating associations: scuba divers with PFOs are more susceptible to decompression illness. Platypnea-orthodeoxia is a condition of desaturation that occurs when you're standing up but not when you're lying down; these patients are quite symptomatic, with arterial saturations in the low 80s. They also frequently have PFOs; if you close the PFO, the arterial desaturation is alleviated. Fat emboli during orthopedic surgery or air emboli during neurosurgery may also travel through the venous system. If you don't have a PFO, the fat or the air is trapped in the lungs and doesn't cause much of a problem unless it's massive; but if you have a PFO, then the embolus can go from right to left atrium up to the brain, with devastating neurologic consequences.

Cardiac Surgical Procedures↗

PubMed1999

Bupropion mimics a transient ischemic attack.

OBJECTIVE: To report the development of symptoms suggesting transient ischemic attacks during bupropion treatment for smoking cessation. CASE SUMMARY: A 67-year-old white man experienced paresthesia, dizziness, tinnitus, confusion, and gait impairment shortly after starting bupropion as an aid to smoking cessation. Bupropion was discontinued on hospital admission, and testing for vertebral basilar artery disease was negative. His symptoms resolved, and he remained asymptomatic until restarting bupropion two days after hospital discharge. DISCUSSION: Although separate case reports have reported sensory disturbances, tinnitus, and balance impairement associated with bupropion use, the combination of symptoms occurring in this patient has not been previously published. CONCLUSIONS: The temporal relationship between bupropion exposure and symptomatology suggests that bupropion caused symptoms mimicking transient ischemic attacks in this patient.

Aged↗

PubMed1991

The Willis lecture: transient ischemic attacks, scientific method, and new realities.

First described by Thomas Willis in 1679 and defined in the 1950s, transient ischemic attack is universally agreed to be an episode of focal neurologic deficit in a vascular distribution, sudden in onset and resolving without residual deficit in less than or equal to 24 hours. Transient ischemic attack is diagnosed by characteristic history and absence of residua on neurologic examination. After these criteria had been accepted, regional cerebral blood flow and computed cranial tomography in the 1970s, later positron emission tomography, and even more recently, magnetic resonance imaging reveal prolonged pathophysiologic and metabolic disturbances even in persons with all the definitional characteristics of transient ischemic attack. These persistent abnormalities necessitate reexamination of the validity of the concept of transient ischemic attack. Furthermore, our group suspects that transient ischemic attack is probably only a marker, and not itself the risk factor, for the cerebral infarction which frequently follows transient ischemic attack. Additionally, the surprising frequency with which cerebral infarction, unrecognized by patient or physician, is revealed using neuroimaging techniques has created a need to redefine the categories heretofore used for diagnosis and assessment of therapy and prognosis for transient ischemic attack and cerebral infarction.

Algorithms↗