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PubMed1988

Transient ischemic attacks and stroke.

Transient ischemic attacks (TIAs) constitute the most specific and powerful warnings of impending stroke. They are defined as brief, focal neurological events of sudden onset. Their proper recognition and treatment rank second only to the modification of risk factors in importance for stroke prevention. Carotid endarterectomy, although widely used to treat TIAs, remains unproven; randomized clinical trials are attempting to define its role. Anticoagulant therapy appears worth while for suspected cardiac embolism and possibly for disabling TIAs. Acetylsalicylic acid is the only agent that has been found to be effective in controlled trials, but questions persist about its dosage, its efficacy in women and its use after stroke. Another platelet inhibitor, ticlopidine hydrochloride, is being investigated and may prove to be an effective alternative.

Aspirin↗
PubMed2004

Transient ischemic attacks before ischemic stroke: preconditioning the human brain? A multicenter magnetic resonance imaging study.

BACKGROUND AND PURPOSE: We investigated whether transient ischemic attacks (TIAs) before stroke can induce tolerance by raising the threshold of tissue vulnerability in the human brain. METHODS: Sixty-five patients with first-ever ischemic territorial stroke received diffusion- and perfusion-weighted MRI within 12 hours of symptom onset. Epidemiological and clinical data, lesion volumes in T2, apparent diffusion coefficient (ADC) maps and perfusion maps, and cerebral blood flow and cerebral blood volume values were compared between patients with and without a prodromal TIA. RESULTS: Despite similar size and severity of the perfusion deficit, initial diffusion lesions tended to be smaller and final infarct volumes were significantly reduced (final T2: 9.1 [interquartile range, 19.7] versus 36.5 [91.2] mL; P=0.014) in patients with a history of TIA (n=16). This was associated with milder clinical deficits. CONCLUSIONS: The beneficial effect of TIAs on lesion size in ADC and T2 suggests the existence of endogenous neuroprotection in the human brain.

Blood Flow Velocity↗
PubMed2005

Ischemic preconditioning as induction of ischemic tolerance after transient ischemic attacks in human brain: its clinical relevance.

Ischemic preconditioning has been well-established in different animal models of cerebral ischemia. Suggesting that transient ischemic attack (TIAs) may represent a clinical model of ischemic tolerance, patients with ipsilateral TIA before ischemic stroke may have a better neurological outcome compared to patients without TIA before ischemic stroke. A retrospective case-control study. Analysis of clinical and neuroradiological findings of 130 patients treated with local intra-arterial thrombolysis using urokinase after ischemic stroke between January 2000 and May 2002. Eleven patients (8%) demonstrated prestroke ipsilateral TIA in the same vascular territory. Despite no significant differences in baseline characteristics, independence (modified Ranking Scale score) and neurological outcome (NIHS score) were significantly associated with prior TIA in multivariante models. Patients with prestroke TIA, showing a similar clinical picture (NIHS score) on admission, demonstrated a more favorable outcome (NIHS score (p<0.001) and modified Ranking score (p<0.0001)) compared to patients with unheralded ischemic stroke. The interval between TIA and ischemic stroke (1-7 days), duration of TIAs (0-20 min) and number of TIAs (2-3) influenced the better outcome in this patients' subgroup. In addition, we could show an induction of ischemic tolerance by prestroke ASA treatment in patients without previous new-onset TIA. Two to three ipsilateral TIA of the same vascular territory and of up to 20 min duration within 1-7 days may lead to ischemic tolerance to a subsequent ischemic stroke as demonstrated by significantly diminished infarct extention throughout all cortical imagines in neuroradiological studies. The role of ASA has to been further elucidated.

Case-Control Studies↗
PubMed2004

Ischemic preconditioning from transient ischemic attacks? Data from the Northern California TIA Study.

Reduced impact of ischemia after an initial ischemic insult-ischemic preconditioning-has been demonstrated in a number of animal models. Transient ischemic attack (TIA) may produce ischemic preconditioning in people who have a subsequent stroke within days of an initial ischemic insult. We performed a cohort study of all 1707 patients given a diagnosis of TIA by an emergency department physician in 1 of 16 hospitals in a managed care plan in Northern California from March 1997 to February 1998. We evaluated the impact of the timing and duration of TIA on disability in a cohort of 180 patients with TIA and subsequent ischemic stroke within 90 days of the TIA. There was no association between duration of TIA, used as a surrogate for degree of ischemia, and likelihood of disability from a subsequent stroke. Furthermore, there was no difference in rates of disability among patients with strokes occurring within 1 day, 1 to <7 days, and 7 to 90 days after the TIA. We cannot confirm results of several other studies showing an association of prior TIA with lesser stroke severity. Whether differences in underlying pathophysiology and treatment of those with prior TIA could account for differences in outcome of subsequent strokes in prior studies is unknown. Evaluating whether ischemic preconditioning occurs after TIA is extremely difficult in observational studies in humans. Given the potential hazards of inducing therapeutic transient brain ischemia in humans, a trial may not be advisable, and proof may require testing of agents that safely mimic the effects of ischemia.

Cohort Studies↗
PubMed1989

[Difference in susceptibility between auditory and equilibrium function in rabbits with experimentally-induced transient ischemic attack].

Patients with transient ischemic attack (TIA) in the vertebrobasilar artery more often complain of disturbance of equilibrium, such as vertigo or dizziness, than of auditory disorders, such as hearing impairment or tinnitus. The author induced TIA in rabbits by injecting adenosine diphosphate (ADP) into the right vertebral artery. Observations of rotatory nystagmus have shown that a peak level of directional preponderance appeared 1 minute after injection of ADP (0.3mg/kg b.w.) and continued for more than 4 minutes. On the other hand, the amplitude of auditory brainstem responses (ABRs) presented no significant changes following the injection of ADP (0.5mg/kg b.w.). However, greater amounts of ADP (1.0 and 2.0 mg/kg b.w.) were found to reduce the amplitude of ABR-waves, although significant reduction was observed for only less than 1 minute. This change was represented by flattening of the later part of the waves, with the first wave much less affected. Electrocochleogram (E. Coch. G.) have also demonstrated a transient reduction in amplitude 10 seconds after injection of ADP (4.0mg/kg b.w.) with correspondingly rapid recovery. In cases of hypertension due to noradrenaline load or trimethaphan-induced hypotension, reduced amplitudes were more profound and continued longer, returning to its normal range within 1 minute. Differences in susceptibility between the equilibrium system and auditory system in TIA of the vertebrobasilar artery are discussed.

Animals↗
PubMed2006

Ischemic preconditioning is mediated by erythropoietin through PI-3 kinase signaling in an animal model of transient ischemic attack.

Ischemic preconditioning (IP) protects the brain from subsequent, prolonged, and lethal ischemia in experimental studies. Erythropoietin (EPO) participates in the brain's intrinsic response to injury and may play a role in preconditioning. By using a middle cerebral artery occlusion (MCAo) model of transient ischemic attack (TIA), we sought to determine whether EPO is required for IP in the protective response against focal ischemic stroke. Rats underwent three 10-min MCA occlusions or sham surgery. Three days later, animals underwent 2 hr of MCAo and 22 hr of reperfusion. Experimental TIAs reduced infarct volumes by 55% (P < 0.05), inhibited DNA fragmentation, and improved neurological outcome by 50% (P < 0.05) after ischemic stroke. EPO and its receptor were up-regulated by IP in the ipsilateral hemisphere by 24 hr after IP, before ischemic stroke and soluble EPO receptor attenuated neuroprotection by IP (88% reduction, P < 0.05). Pretreatment with the PI-3 kinase inhibitor wortmannin abolished the protective effect of IP against ischemic injury (P < 0.05). IP may be mediated in part by EPO through a PI-3 kinase pathway.

Animals↗
PubMed1986

Clinical predictors of cardiac and arterial lesions in carotid transient ischemic attacks.

In 205 patients with carotid transient ischemic attacks (TIAs) who underwent full angiographic and cardiac investigations, we found that ipsilateral carotid bruit and triggering of TIA by exertion or standing up suggested a carotid lesion. Angina pectoris or palpitations at onset of TIA suggested a cardiac source of emboli. Patients with only one TIA, multiple identical attacks, progression of symptoms over minutes, and appropriate infarct on computed tomograms (28%) were likely to show a potential arterial or cardiac cause for the TIAs in subsequent investigations. Transient monocular blindness correlated with carotid occlusion, but the severity of the carotid lesion did not influence the duration and repetition of attacks. Transient ischemic attacks in multiple territories, identical attacks, and multiple or silent infarcts on computed tomograms occurred equally in the patients with arterial lesions and those with cardiac lesions. These findings suggest that only a few, albeit important, conclusions regarding etiology can be drawn from the clinical characteristics of TIAs.

Adult↗
PubMed2002

Neuroprotection and P450 2C11 upregulation after experimental transient ischemic attack.

BACKGROUND AND PURPOSE: Transient ischemic attack (TIA) is a risk factor for stroke. However, TIA may also serve as a preconditioning stimulus, reducing damage from subsequent stroke. We tested the hypothesis that experimental TIA induces expression of P450 2C11, an arachidonic acid epoxygenase that produces vasodilator epoxyeicosatrienoic acids, leading to increased tissue perfusion and reduced stroke damage. METHODS: Wistar rats underwent three 10-minute middle cerebral artery occlusions (TIA) or sham surgery. Three days later, animals were subjected to 2-hour middle cerebral artery occlusion and 24 hours of reperfusion. Brains were stained with 2,3,5-triphenyltetrazolium chloride for infarct size measurement or processed for quantification of P450 2C11 mRNA and protein with the use of RNase protection assay and Western blotting. Regional cerebral blood flow (CBF) at the end of 2-hour ischemia was measured in separate groups of rats with iodoantipyrine autoradiography. RESULTS: Cerebral infarct was reduced by >50% in TIA- versus sham-preconditioned animals. 2C11 mRNA and protein were increased in ipsilateral hemisphere by 3 days after TIA but not sham surgery. Induction of 2C11 by TIA was also evident in ipsilateral hemisphere at 24 hours after 2-hour middle cerebral artery occlusion and 24 hours of reperfusion. End-ischemic regional CBF was not different between TIA- and sham-pretreated groups. CONCLUSIONS: We conclude that experimental TIA induces ischemic tolerance by a mechanism temporally linked to upregulation of P450 2C11. Enzyme induction does not attenuate ischemic severity by amplifying end-ischemic CBF.

Animals↗
PubMed1998

Direct costs of transient ischemic attacks: a hospital-based study of resource use during the first year after transient ischemic attacks in Denmark.

BACKGROUND AND PURPOSE: Knowledge of costs of health care and social services for patients who have transient ischemic attacks (TIAs) is scarce. This study investigates the resource use and estimates direct costs during the first year after a TIA. METHODS: All patients admitted to a university hospital in Copenhagen, Denmark, because of TIA during 12 months in 1994-1995 were included in a database. The patients were followed until 1 year after admission, and data on resource use during and after the hospital stay were collected prospectively at interviews. RESULTS: The cost of the hospital stay had a mean of DKr 10100 (US $1800), and the cost of health care and social services after discharge had a mean of DKr 8800 (US $1600). CONCLUSIONS: The total cost of health care and social services during the first year after a TIA had a mean of DKr 18800. The hospital stay and the services after discharge each made up half of the total direct cost.

Adult↗
PubMedDate not supplied

[A study of the risk factors in transient global amnesia and its differentiation from a transient ischemic attack].

INTRODUCTION: Transient global amnesia (TGA) is a clinical condition that has been described in many studies, but its pathophysiology is not fully understood. In recent years the theory of valvular insufficiency in the jugular vein has been added to the classical hypotheses that link it to migraine, to epilepsy and -the most widely accepted- to transient ischemic attacks (TIA), although the real origin of the condition has still not been determined. PATIENTS AND METHODS: In a retrospective study we compared 131 patients diagnosed with TGA between 1993 and 2004 with 262 patients who were diagnosed as having TIA over the same period. RESULTS: Mean age was 65.94 years in TGA versus 71.11 years in the case of TIA. There was a higher rate of arterial hypertension among the patients with TGA and diabetes mellitus was more frequent among those with TIA (p<0.05 in both cases). Emboligenic heart disease was scarce among patients with TGA. The number of patients with a history of ischaemic heart disease and a history and the development of cerebrovascular diseases was greater among those with TIA than in cases of TGA (p<0.05). The TGA recurrence rate was 12%. The percentage of pathological findings in the CAT brain scan was higher in patients with TIA (p<0.05). There are no significant differences between patients with TGA and TIA as far as treatment on hospital discharge is concerned. CONCLUSIONS: TGA does not seem to be a symptom of an arteriosclerotic pathology nor does it appear to offer a higher risk of heart or cerebrovascular disease and, therefore, antiaggregating therapy would not be indicated in such cases.

Aged↗
PubMed1991

Transient ischemic attacks with and without a relevant infarct on computed tomographic scans cannot be distinguished clinically. Dutch Transient Ischemic Attack Study Group.

We prospectively studied clinical and computed tomographic (CT) scan findings in 79 patients with a transient ischemic attack (TIA) and a relevant cerebral infarction on CT, also known as cerebral infarction with transient signs (CITS). We compared the results with those of 527 concurrent patients with TIA and without cerebral infarction and also with 646 patients with persistent neurological symptoms and a relevant infarct on CT. All patients were participating in a multicenter trial. In both groups, most infarcts were of the lacunar type. Compared with TIAs without cerebral infarction, patients with CITS slightly more often had a history of hypertension (52% vs 33%), the attacks lasted longer (greater than 1 hour, 52% vs 34%) and disappeared more slowly (over the course of hours, 39% vs 24%), and the symptoms more frequently involved speech (61% vs 41%). Despite these small differences, the reverse--the prediction of evidence on CT of infarction on the basis of the nature or time course of symptoms--proved impossible, since in each category the majority of patients had a normal CT scan. In comparison with patients with stroke and visible infarction, patients with CITS slightly more often had abnormal speech (61% vs 45%) and had a larger number of attacks (multiple attacks, 46% vs 18%). In conclusion, we found only minor clinical differences between patients with TIA with or without a relevant infarct on CT and equally small differences between patients with CITS and patients with stroke and cerebral infarction. These clinical similarities do not exclude a difference in prognosis.

Cerebral Infarction↗
PubMed1977

Cooperative study of hospital frequency and character of transient ischemic attacks. VI. Patients examined during an attack.

Examination during an episode of transient ischemic attack (TIA) was performed on 121 of 1,307 patients suspected of having a single type of TIA. This examination supported the diagnosis of TIA in 79 patients and contributed to the establishment of a diagnosis other than TIA in 42. Although the examination increased diagnostic reliability, it did not always result in a definite diagnosis. The most common neurologic findings during a TIA were weakness of an arm or side of the face. Important findings not suggested by history included visual defects and blood pressure fluctuation. Also unexpected were the absence of findings such as sensory deficits in the presence of sensory complaints, retinal emboli, and cardiac abnormalities. Severe arteriosclerotic disease was less evident, the attacks were longer and more severe, and monocular blindness was rare.

Acute Disease↗
PubMed1992

Silent stroke in patients with transient ischemic attack or minor ischemic stroke. The Dutch TIA Trial Study Group.

BACKGROUND AND PURPOSE: We studied silent stroke (i.e., infarcts on computed tomographic scan not related to later symptoms) in patients after transient ischemic attack or minor ischemic stroke. METHODS: Ours is a cross-sectional study of 2,329 patients who were randomized in a secondary prevention trial after transient ischemic attack or minor ischemic stroke and had no residual deficit after the qualifying event. RESULTS: Silent stroke was observed in 13% of the 2,329 patients. Lacunes formed 79%, cortical lesions 14%, and border zone lesions 7% of all silent strokes. Silent lacunes were most often located in the basal ganglia and symptomatic lacunes most often in the corona radiata. Age, hypertension, and current cigarette smoking were related to the presence of silent stroke. Silent stroke was equally common in different types of transient ischemic attack, including transient monocular blindness. Residual symptoms of any kind were more common in patients with silent stroke than in those without. CONCLUSIONS: Because only the sites of silent stroke infarcts differed slightly from those of symptomatic infarcts and the frequency of vascular risk factors was similar to that of symptomatic infarcts, silent stroke may have the same bearing on future risk as known prior stroke.

Cerebrovascular Disorders↗
PubMed1983

Transient ischemic attacks.

Patients with transient cerebral ischemic attacks (TIAs) are generally felt to be at increased risk for stroke. A comprehensive clinical evaluation consisting of a thorough history and physical examination, as well as adjunctive laboratory and radiologic studies, is required to substantiate the diagnosis and to identify the underlying etiology. For patients with TIAs of atherothrombotic origin, the optimal course of management is still controversial. Although surgical therapy, antiplatelet therapy, and anticoagulant therapy have all shown promise in preventing stroke, their precise roles in the management of TIAs still await further elucidation.

Aged↗