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PubMed1987

Course of blood pressure after cerebral infarction and transient ischemic attack.

In 63 patients, admitted for cerebral infarction or transient ischemic attack (TIA), the blood pressure course was studied. The blood pressure before the event was studied retrospectively; 32 patients were normotensive, in 31 patients existed hypertension, with antihypertensive treatment in 15 of these cases. The blood pressure after the event was studied prospectively, and turned out to be risen in 67% of the patients on the day of admission. It fell in the first day after infarction or TIA, mainly on the second day, to a plateau level reached on the fifth day. Only 3 patients (5%) remained hypertensive until discharge from the hospital. In 48 patients blood pressure values were available as measured two to six months after discharge, without a change in antihypertensive medication. Blood pressure was increased compared to the value measured before discharge. In 14 patients (29%) hypertensive blood pressure figures were measured at that time. It is concluded that blood pressure is elevated in the acute phase of cerebral infarction and TIA, but falls spontaneously in the first days to normotensive levels in most patients; because blood pressure may increase again, measurements of blood pressure within the first months after discharge are needed.

Aged↗
PubMed2005

Transient ischemic attack: a dangerous Harbinger and an opportunity to intervene.

Transient ischemic attack (TIA) and ischemic stroke are both characterized by sudden onset of neurological symptoms due to focal cerebral ischemia, but they are distinguished by the duration of neurological symptoms, with TIA traditionally defined by resolution of symptoms within 24 hours and stroke reserved for symptoms of longer duration. Because TIA and ischemic stroke share etiologies, it is not surprising that the recommended evaluations and secondary prophylaxis are identical. However, recent studies suggest that optimal management of TIA and stroke may differ more than previously recognized. The short-term risk of ischemic stroke after TIA is very high, which may be because rapid recovery from neurological symptoms is indicative of reversal of ischemia and tissue still at risk. Regardless of whether residual symptoms or infarction are present, rapid recovery appears to predict a greater short-term risk of subsequent ischemic stroke and is more likely to reflect a distinct, unstable pathophysiology. Therefore, it may be more useful to characterize acute ischemic cerebrovascular syndromes on the basis of the extent of rapid recovery (i.e., on the inferred reversal of ischemia) than on the completeness of recovery at 24 hours. Patients with substantial rapid recovery may be those for whom acute intervention is most warranted.

Cerebral Infarction↗
PubMed1986

The long-term results of carotid endarterectomy for transient ischemic attacks.

One hundred patients who underwent carotid endarterectomy for transient ischemic attacks (TIAs) have been followed up for 3 to 10 years (mean, 5.5 years). Seven patients have been lost to follow-up but none is recorded as dead (National Registry of Deaths) at least 5 years after operation. Fifteen patients (16.5%) have died, four from cerebral and eight from cardiac causes. Three patients had cerebral infarction with permanent deficits, one occurring immediately after operation, one at 3 months, and one at 9 years. Four patients had minor strokes but a full clinical recovery, three patients postoperatively and one patient at 4 years. Fourteen patients had ipsilateral TIAs, four occurred postoperatively and 10 occurred from 1 to 8 years later. Ten patients had contralateral TIAs and five patients then had a contralateral carotid endarterectomy. Another nine patients also had bilateral operations, three for bilateral TIAs, five as prophylactic procedures on the basis of arteriographic findings, and one for a contralateral cerebral event that occurred after arteriography. Thus, at the mean follow-up time (5.5 years) and including the operative complications, four deaths (4%) of cerebral origin and seven serious cerebral problems (7%) have occurred--an annual morbidity and mortality rate of less than 2%. This compares favorably with the commonly predicted rate of stroke occurring after TIAs of 5% per year. These figures support the argument that carotid endarterectomy reduces the incidence of stroke occurring after TIA and stops TIAs caused by emboli from the carotid bifurcation.

Adult↗
PubMed1981

Transient ischemic attacks: differentiation and treatment.

Several options exist for treating transient ischemic attacks (TIAs), although none can eliminate the risk of cerebral infarction. For carotid TIA, carotid endarterectomy is the preferred therapy in patients with an angiographically demonstrated sclerotic lesion, whereas extracranial-intracranial bypass may be beneficial in patients with carotid artery occlusion or intracranial arterial stenosis. For patients who are not surgical candidates, oral anticoagulants may be helpful, but hemorrhagic complications can occur. Control of risk factors (especially hypertension) and associated medical conditions (especially heart diseases) is necessary. Many unanswered questions about ischemic cerebrovascular disease persists. Further studies and research are necessary.

Diagnosis, Differential↗
PubMed1984

Transient ischemic attacks. Strategies for minimizing stroke risk.

In patients with transient ischemic attack (TIA), the risk of stroke increases greatly, especially in the months immediately following the initial attack. Diagnosis of TIA is based primarily on the patient's cerebrovascular history, since results of neurovascular examination are usually normal. TIA is often related to atherosclerotic arterial disease but can have numerous causes. Migraine, focal seizures, and other neurologic conditions can closely mimic TIA. Surgical and medical therapies help minimize the risk of stroke. The choice of therapy depends on the vascular territory of ischemia, the cause of the attack, the patient's medical and neurologic condition, the availability of a skilled surgeon, and other factors.

Aged↗
PubMed1999

Practice variability in management of transient ischemic attacks.

To define practice patterns in the management of transient ischemic attacks (TIAs), we surveyed practicing neurologists attending an educational conference in San Francisco, evaluating management decisions in 2 TIA case vignettes. In a vignette describing a hemispheric TIA 1 day prior with ipsilateral bruit, 53% chose admission, 47% elected an outpatient work-up, 28% treated with intravenous heparin and 70% chose aspirin, reflecting the disagreement about medical management of carotid stenosis in the literature. There was more agreement in the second case, a posterior circulation TIA 1 day prior with atrial fibrillation, in which 84% chose hospital admission, 74% chose intravenous heparin and 90% treated with some form of anticoagulation. There are areas of important practice variability in the management of TIAs. Further research is justified to guide patient care decisions in TIA patients.

Aged↗
PubMedDate not supplied

Outcome of surgical treatment of 110 patients with transient ischemic attack.

Between 1980 and 1982, 227 consecutive patients with transient ischemic attack (TIA) or ischemic brain infarction (IBI) were evaluated as possible candidates for carotid surgery in the Department of Neurology, University of Helsinki. One hundred and ten patients (mean age 58, range 41-72 years) were selected for surgery; 82 of them had had TIA and 28 IBI as the presenting symptom. After a total of 128 operations (84 unilateral and 18 bilateral endarterectomies, and 8 arterial reconstructions), 16 patients (14.5%) developed neurological deficits. In 7 patients (6.4%), the deficit was severe and 4 of them (3.6%) died within the first four days after surgery. Ten patients had occlusion of the contralateral internal carotid artery and/or severe hypertension. Five of them suffered ischemic brain infarction after the operation and two died. Operation on an occluded internal carotid artery in 7 patients was complicated by hemiparesis in two patients, one of whom died. Patients with surgical complications more often had severe hypertension (p less than .001), total occlusion of the contralateral internal carotid artery, (n.s.) and severe angiographic changes (n.s.) compared with patients without complications. During the follow-up the annual rate for IBI was 3.3% and for acute myocardial infarction (AMI) 4.4%. Vascular death occurred with a frequency of 1.7% per year. The results emphasize that patients with TIA or IBI should be carefully evaluated before recommending surgical treatment for prevention of threatened stroke. Patients with severe risk factors may fare better on medical treatment than with surgical intervention.

Adult↗
PubMedDate not supplied

Factors influencing the survival of 451 transient ischemic attack patients.

Four hundred fifty-one patients with transient ischemic attacks (TIA) occurring within 1 month of hospitalization, admitted during 1977-1983, were analyzed to establish the effect on survival of age, race, sex, distribution of TIA, cigarette smoking, previous cerebral infarction or hemorrhage, previous TIA, or history of ischemic heart disease, valvular heart disease, cardiac dysrhythmia, hypertension, and diabetes mellitus. Proportional hazards analysis revealed that decreased survival was associated with increasing age, carotid artery distribution TIAs (compared with vertebrobasilar distribution TIAs), cigarette smoking, previous contralateral stroke, ischemic heart disease, and diabetes mellitus. We found great variation in the estimated survival of TIA patients, ranging from 5-year survivals of greater than 95% for 60-year-old patients with none of these risk factors to less than 25% for patients with all of these risk factors. Although the survival of the strata differed, the average mortality rates for this series of patients was about one-half of that observed for 225 patients accessed and followed by our center during 1961-1973.

Aged↗
PubMed1989

SPECT study of cerebral blood flow reactivity after acetazolamide in patients with transient ischemic attacks.

We investigated 15 patients with one or more transient ischemic attacks (TIAs) in the internal carotid artery territory within the month following the most recent TIA. Cerebral blood flow (CBF) was measured by single-photon emission computed tomography, using intravenous xenon-133 before and after injection of 1 g acetazolamide. Six patients had severe carotid stenosis or occlusion; the other nine patients had no significant carotid lesions. Twenty age-matched volunteers free of neurologic symptoms or history were used as controls. Mean CBF in the sylvian region was not significantly different between patients and controls. Seven patients exhibited a focal hypoperfusion at rest in the symptomatic hemisphere, and their hypoperfused areas were hyporeactive after administration of acetazolamide. Seven other patients exhibited hyporeactive areas after acetazolamide administration while their CBF tomograms at rest were normal. Thus, CBF abnormalities were detected in 14 of the 15 patients. Our findings suggest that CBF measured early after acetazolamide administration could be useful to confirm the clinical diagnosis of TIA. In the nine patients with no significant lesion of the internal carotid artery, the areas of hypoperfusion were small and were probably related to the focal ischemic event. In the six patients with severe lesions of the internal carotid artery, abnormalities were of variable size and intensity but were often large and pronounced. The discrepancy between these two subgroups of patients could be ascribed to the hemodynamic influence of the internal carotid artery lesions. Moreover, our findings may provide some insight into the pathophysiology of TIAs.

Acetazolamide↗
PubMed1985

Headache in transient ischemic attacks (TIA).

The evaluation of headache in patients with transient ischemic attacks (TIA) has various sources of difficulty, the definition of TIA being the most relevant. The classical definition needs to be supplemented with a normal CT scan if a misleading diagnostic statement is to be avoided. The clinical features of 90 patients suffering from TIA and who had contrast-enhanced CT scans are reported. Headache occurred in 30% of the patients. Headache prevailed in patients with vertebrobasilar TIA compared with carotid TIA (p less than 0.05). Headache prevailed as a preceding (24 h) and/or concomitant sign compared with other neurological symptoms (77.8% of the patients). Headache was ipsilateral, in the anterior half of the head in the carotid TIA and in the posterior half of the head in the vertebrobasilar TIA. In about 50% of the patients generalized non-localized headache occurred. Headache usually preceded the neurological symptoms in cases of arterial occlusion (20 carotid, 3 vertebral artery), usually appearing during or after the attack in cases without arterial occlusion. Only 2 cases out of 20 with positive CT scan had headache. These two patients suffered from a rather large hypodense lesion. The other 18 patients showed lacunar lesions. Different hypotheses concerning the physiopathology of the headache associated with TIA are discussed.

Adult↗
PubMed2004

Early risk of stroke after a transient ischemic attack in patients with internal carotid artery disease.

BACKGROUND: Transient ischemic attacks (TIAs) often herald a stroke, but little is known about the acute natural history of TIAs. Our objective was to quantify the early risk of stroke after a TIA in patients with internal carotid artery disease. METHODS: Using patient data from the medical arm of the North American Symptomatic Carotid Endarterectomy Trial, we calculated the risk of ipsilateral stroke in the territory of the symptomatic internal carotid artery within 2 and 90 days after a first-recorded hemispheric TIA. We also studied similar outcomes among patients in the trial who had a first-recorded completed hemispheric stroke. RESULTS: For patients with a first-recorded hemispheric TIA (n = 603), the 90-day risk of ipsilateral stroke was 20.1% (95% confidence interval [CI] 17.0%-23.2%), higher than the 2.3% risk (95% CI 1.0%-3.6%) for patients with a hemispheric stroke (n = 526). The 2-day risks were 5.5% and 0.0%, respectively. Patients with more severe stenosis of the internal carotid artery (> 70%) appeared to be at no greater risk of stroke than patients with lesser degrees of stenosis (adjusted hazard ratio 1.1, 95% CI 0.7-1.7). Infarct on brain imaging (adjusted hazard ratio 2.1, 95% CI 1.5-3.0) and the presence of intracranial major-artery disease (adjusted hazard ratio 1.9, 95% CI 1.3-2.7) doubled the early risk of stroke in patients with a hemispheric TIA. INTERPRETATION: Patients who had a hemispheric TIA related to internal carotid artery disease had a high risk of stroke in the first few days after the TIA. Early risk of stroke was not affected by the degree of internal carotid artery stenosis.

Aged↗
PubMedDate not supplied

[Modifiable risk factors for non-cardioembolic transient ischemic attacks. Case control studies in the general population].

INTRODUCTION: Transient ischemic attacks (TIA) often precede a stroke. AIMS: The purpose of this study is to examine the modifiable cardiovascular risk factors for non-cardioembolic TIA. PATIENTS AND METHODS: A population based case control study was conducted in a district within the city of Barcelona. The cases were 103 patients with non-cardioembolic TIA, who had been diagnosed by a neurologist, and with normal CAT or MRI scans. Subjects were paired by age and sex with 193 controls without TIA or stroke, who were selected by simple random sampling from the clinical records file at the centre. The risk factors were studied using a standardized questionnaire that included the following factors which were codified in a dichotomous manner: smoking, arterial hypertension (AHT), hypercholesterolemia, hypertriglyceridemia, obesity, impaired fasting glucose and diabetes mellitus (DM). RESULTS: The average age was 74.6 years and 52.3% of the subjects were females. All the modifiable cardiovascular risk factors were associated to a higher risk of TIA, although only AHT (OR: 1.9; CI 95%: 1.1-3.3) and obesity (OR: 2.1; CI 95%: 1.2-3.6) were associated in a significant way in the univariate analysis. In the multivariate analysis by logistic regression, the modifiable cardiovascular risk factors that were associated in a significant manner were AHT (OR: 1.9; CI 95%: 1.0-3.6), obesity (OR: 2.8; CI 95%: 1.4-12.3) and DM (OR: 1.7; CI 95%: 1.0-2.9). CONCLUSIONS: In the present study, AHT, obesity and DM were seen to be modifiable risk factors for non-cardioembolic TIA.

Case-Control Studies↗
PubMed2005

[Transient ischemic attacks in the elderly: new definition and diagnostic difficulties].

Transient ischemic attacks (TIA) are very frequent in the elderly. Their frequency increases beyond 65 years. However, no epidemiologic study was specifically dedicated to elderly patients. The first definition of TIA was a sudden focal neurologic deficit that lasted for less than 24 hours, presumed to be of vascular origin and located in a specific artery territory of the brain or eye. The Working Study Group has proposed a new definition: TIA is a brief episode of neurologic dysfunction caused by focal brain or retinal ischemia with clinical symptoms typically lasting less than one hour, most often some minutes, and without evidence of acute infarction. Weighted diffusion MRI may show very early an aspect of cytotoxic oedema. The one-hour criterion associated with a stable neurological deficit is requested for initiating IV thrombolysis, if the angio-MRI shows an occlusion of the supra-aortic trunks or intracranial arteries, even in aged patients. Each TIA constitutes a major risk for a completed infarct resulting in disability or death. Hypertension is the main risk factor for TIAs, followed by atrial fibrillation, diabetes, coronaropathy and sedentarity. These factors multiply by 4 the stroke risk. In the elderly, TIAs are pecularly associated with lacunar infarcts in the territory of deep perforating arteries. TIAs represent a neurologic emergency that allows no delay in clinical and laboratory investigations, such as ultrasonic echographies and weighted diffusion MRI. Diagnostic errors are often due to frequent polypathology and cognitive changes in great age. The most misleading symptoms are vertigo, imbalance, falls, disorders of consciousness. Unawareness of the deficit is also a frequent cause of failure of TIA diagnosis. Conversely, the most frequent cause of diagnostic error by excess is epileptic seizures which are often under-evaluated.

Aged↗
PubMed2006

[Correlation between the polymorphism of platelet glycoprotein GPIb α Kozak gene and transient ischemic attack].

OBJECTIVE: Genic susceptibility could increase the risk of transient ischemic attack (TIA). The objective of this study is to investigate the relationship between the polymorphism of platelet glycoprotein GPIb α Kozak gene and TIA in Qindao Han population. METHODS: The polymorphisms of platelet glycoprotein GPIb α Kozak gene -5T/C in TIA patients and normal control were detected with sequence-specific primers polymerase chain reaction (PCR-SSP). RESULTS: The prevalence of the CC genotype and C alleles were significantly higher in TIA patients than in the control group (P<0.05). The positive correlation between C allele and TIA was showed by logistic regression analysis (P=0.016). CONCLUSION: The -5T/C polymorphism of the platelet glycoprotein GPIb α Kozak gene is implicated in the pathogenesis of TIA. C allele is an independent risk factor for TIA.

Aged↗
PubMed1989

[Treatment of transient ischemic attack by carotid endarterectomy].

Fourty-five patients with transient ischemic attack (TIA) were treated by carotid endarterectomy. All of them had typical manifestation of TIA and stenosis of extracranial carotid artery verified by angiography. After operation most of them were uneventful, but 2 experienced TIA, 2 contralateral reversible weakness and 1 mild hoarseness. There was no mortality. The role of carotid endarterectomy in the prevention and treatment of TIA, and some technical factors including anesthesia, intraoperative monitoring, management of stenosis of high subcranial internal carotid artery and postoperative care, were discussed.

Adult↗
PubMed1985

[Cerebral hemorrhage complicating early anticoagulant treatment of transient ischemic attacks].

Two patients received intravenous heparin shortly after carotid transient ischemic attacks (TIAs), and developed a cerebral hemorrhage in the same area with 24 hours. CT scan performed before starting anticoagulation was normal, blood pressure was not too high when the hemorrhage developed, although the patients suffered (treated) chronic hypertension, and the Partial Thromboplastin Time did not exceed 90 seconds. No definitive explanation can be provided for this severe complication but recent studies suggest that in some TIAs, significant local ischemic changes may persist after the resolution of clinical symptoms. This risk, although very low, should be considered in cases with chronic arterial hypertension (even treated), because of disturbances of cerebrovascular regulation. In the near future, nuclear magnetic resonance scanning might allow detection of the cases with TIAs, in which focal metabolic alterations persist after disappearance of clinical symptoms.

Aged↗
PubMed1994

Transient ischemic attacks: diagnosis, and medical and surgical management.

Patients experiencing transient ischemic attacks (TIAs) may have a 2-year stroke rate as high as 57%, and carotid endarterectomy has been shown in prospective randomized studies to be highly effective in reducing this rate. Therefore, it is crucial to correctly identify patients with TIAs, treat underlying causes appropriately, and identify those most likely to benefit from endarterectomy. Whether in the anterior or posterior circulation, TIAs are focal neurologic events that usually last 5 to 30 minutes and are characterized by an abrupt onset followed by gradual resolution. They may be caused by artery-to-artery thromboembolism, cardiogenic embolism, or thrombosis of a small penetrating cerebral vessel (threatened lacunar infarction). A number of contributing disorders must be considered, including migraine, arterial dissection, vasculitis, thrombotic diatheses, blood dyscrasias, infections, and drug abuse. Carotid endarterectomy should be considered only for patients with hemispheric TIAs in whom lacunar events, cardiogenic embolism, and other underlying causes of stroke have been excluded and ipsilateral carotid stenosis of greater than 70% has been demonstrated. The value of endarterectomy increases: if the patient is relatively willing to take immediate risks in order to avoid future morbid events (low risk aversion) and believes stroke is a serious event, nearly tantamount to death; if the morbidity and mortality of the operation, as determined by institutional audits, is low; and if the degree of carotid stenosis is high. The value of endarterectomy declines rapidly with time elapsed from the TIA. Endarterectomy is of marginal value in patients with amaurosis fugax, of uncertain value in patients with stroke, and unlikely to be of any value in patients with asymptomatic carotid stenosis. Long-term anticoagulation has been shown to be beneficial only in patients at risk for cardiogenic embolism. Others, including those undergoing endarterectomy, should receive aspirin. In all patients, there should be an aggressive effort to control risk factors for cardiovascular and cerebrovascular disease.

Endarterectomy, Carotid↗