Stroke and TIA: Epidemiology, Risk Factors, and the Need for Early Intervention

Published Online: June 15, 2008
Marc Fisher, MD

The risk of recurrent stroke in patients who have suffered a prior stroke or transient ischemic attack (TIA) is significant. It is imperative that individuals who report symptoms of a cerebrovascular event receive immediate medical attention— preferably at a hospital—to help determine its origin and impact. Many researchers recommend that any evaluation include neuroimaging studies to target those patients who would benefit most from secondary prevention, such as antithrombotic therapy.

This article defines the 2 main types of stroke and their respective subtypes and discusses the debate over how to define stroke versus TIA. Additionally, the article talks about the incidence of stroke, related morbidity and mortality rates, and several risk factors that predispose an individual to stroke and recurrent stroke. Several systems have been established to help determine the likelihood of stroke for patients with concurrent risk factors. Measures for secondary prevention can be initiated to address many of these risk factors.

The importance of early intervention cannot be underestimated. Rapid treatment following a stroke or TIA can minimize cerebrovascular damage and prevent recurrence; addressing modifiable risk factors can reduce the risk of subsequent cardiovascular and cerebrovascular events. Facilitating the initiation of effective secondary preventive therapy must become a priority in managed care.

(Am J Manag Care. 2008;14:S204-S211)

Every 40 to 45 seconds someone in the United States suffers a stroke.1,2 One quarter of initial stroke survivors suffer a second stroke within 5 years.2 Long before experiencing a stroke, many people have cerebrovascular risk factors that have not been adequately addressed, such as transient ischemic attacks (TIAs). TIAs are frequently followed by stroke.2,3 Sometimes TIAs remain unidentified because patients did not seek medical attention. TIAs may also be misdiagnosed or go untreated because baseline function returned prior to a medical evaluation.4 Any diagnosed stroke or TIA deserves rapid evaluation and long-term therapy to help prevent further cerebrovascular events.3

Defining Stroke and TIA
Stroke is a neurologic event related to diseases of the cerebral circulation. Symptoms of stroke include sudden severe headache, focal muscular weakness or numbness, impaired vision, dizziness, confusion, or difficulty speaking or understanding speech. Visual loss and weakness or numbness are frequently relegated to one side of the body.

TIAs are briefer episodes of neurologic deficit that occur as a result of focal cerebral or retinal ischemia.5,6 TIAs were once regarded as benign7 but are now recognized as warning signs of underlying cerebrovascular disease with the potential to cause permanent brain injury.3 Most TIAs resolve within 1 hour.3,6,7 Only 2% to 15% of TIAs that fail to resolve within 1 hour will do so within 24 hours.7

Strokes and TIAs previously were diagnosed on the basis of clinical impression alone, and traditional definitions held that TIA should be diagnosed when symptoms persisted for fewer than 24 hours, whereas a completed stroke should be diagnosed when symptoms persisted beyond 24 hours.3,6,7 It was also thought that TIAs left no permanent deficits.7,8

The advent of sophisticated neuroimaging technologies has blurred the line between stroke and TIA.7 Computed tomography (CT) studies from the 1980s to the 1990s found that 15% to 20% of TIA patients had cerebral infarction in areas relevant to symptoms.7 Recently, diffusion-weighted magnetic resonance imaging (DWI) has demonstrated lesions suggestive of permanent ischemic injury in some TIA patients.7 This has led some researchers to propose that the definition of TIA be modified to specify that the condition leaves no evidence of acute infarction on neuroimaging studies.3,5-7 According to this definition, imaging studies that show relevant infarction would indicate stroke, regardless of the duration of symptoms.7

Some researchers recommend that all TIA patients undergo brain imaging urgently—as soon as possible after the onset of symptoms—to identify causes and target secondary prevention efforts.7,9 CT scanning and DWI can demonstrate regions of injury and help to distinguish between hemorrhage, ischemic infarction, and other etiologies, such as tumor.3,5,7,10 DWI can also help differentiate an infarction from penumbra (the region surrounding the ischemic core that is hypoperfused but not yet infarcted).3 In patients who have experienced TIA or a mild-to-moderate ischemic stroke, imaging modalities such as ultrasonography, CT angiography, and magnetic resonance angiography can detect internal carotid artery stenosis,5,9 a condition that may benefit from early treatment with carotid endarterectomy.9

Based on the traditional definition of TIA, some clinicians might delay intervention for 24 hours after symptoms first appear to see whether they subside. Waiting could be problematic in cases where the cause of suspected TIA requires immediate treatment. Also, within this 24-hour window, the patient could experience a completed stroke following TIA.3,4,7 Hospital observation enables immediate intervention if the patient should experience a subsequent stroke.9 Damage in the penumbra of acute ischemic stroke may be reversible, and rapid treatment can prevent it from becoming incorporated into the infarct.10 Prompt thrombolysis can improve outcomes10,11 with an acceptable level of risk for intracranial hemorrhage (ICH), provided proper care is exercised in patient selection.10

TIAs require immediate evaluation, and treatment should be initiated promptly to prevent subsequent stroke.5 Most patients who report TIA-like symptoms should be sent to the emergency department.5 In patients who do not seek medical attention or who are not referred for imaging studies, TIAs serve as unheeded warnings of possible cerebrovascular disease.

Stroke Types and Subtypes
According to the American Stroke Association, approximately 87% of strokes are ischemic and the other 13% are hemorrhagic.1,2 Hemorrhagic strokes are associated with a higher mortality rate,12 which suggests that an even greater proportion of recurrent strokes likely have ischemic etiology.12 Unlike brain hemorrhage, which originates from blood collecting in the extravascular space, ischemic stroke involves the occlusion of blood vessels. In the core zone of ischemia, where blood flow is lower than 10% to 25%, irreversible neuronal damage can occur within minutes.13,14 In the ischemic penumbra, neurons can remain viable for several hours. Rapid restoration of perfusion in this region can save penumbral cells.10

Stroke, especially in younger patients, may be associated with arterial dissection, hypercoagulable states, venous sinus thrombosis, vasculitis, hyperviscosity syndrome, thrombocytosis, sickle cell disease, or patent foramen ovale.6,15 Of all ischemic strokes, ≥15% are cryptogenic (without an identifiable cause).16,17 The etiology of a stroke, when it can be determined, affects treatment decisions, including therapy for secondary stroke prevention. For example, oral anticoagulation is a primary recommended treatment for cardioembolism, antiplatelet therapy is recommended for noncardioembolic ischemic stroke and TIA, and carotid endarterectomy is recommended for recent TIA or minor stroke occurring with severe carotid artery stenosis.6

Hemorrhagic Subtypes
ICH—the presence of blood within the main cellular mass of the brain—accounts for ~10% of all strokes.1 The incidence of ICH due to the use of oral anticoagulants has increased as these therapies have become more prevalent.18,19 In elderly individuals, the deposition of amyloid protein into blood vessel walls may cause hemorrhage. In most cases of ICH, however, chronic hypertension leads to the degeneration of smaller brain arteries and microaneurysms; bleeding originates from tears at the bifurcation between the vessels. The patient’s symptoms may change in relation to additional bleeding and expansion of the affected area; note that rupture of a cerebral artery can cause immediate death.

Subarachnoid hemorrhage (SAH) is the second hemorrhagic subtype and accounts for 3% of all strokes.1 SAH is most prevalent among middle-aged women and has a high mortality rate.15 SAH usually results from the rupture of a cerebral aneurysm at a vessel bifurcation.20 Vasospasm of brain arteries is a common complication of SAH and can lead to a subsequent ischemic brain injury.20

Ischemic Subtypes
There are 3 main subtypes of ischemic stroke, and investigators have used several systems to classify them.21-23 Systems based only on brain imaging exclude patients with a definite ischemic stroke but no visible infarct.22 Other classification systems, such as the ones established by the National Institute of Neurological Disorders and Stroke and TOAST (Trial of Org 10172 in Acute Stroke Treatment), consider brain imaging results plus clinical features.22,23

Large vessel disease (LVD) is a subtype of ischemic stroke. In LVD stroke, slowly developing atherosclerosis can result in the rupture of an intravascular plaque, development of a thrombus, and an embolus in the circulatory system, which can become lodged in part of the brain and obstruct cerebral blood flow.23 Other LVD strokes are caused by stenosis or occlusion of a main artery, which leads to ischemic injury at the farthest branches of the artery; this is called watershed infarction.24 LVD includes strokes caused by aortic arch thromboembolism.25

Lacunar or small vessel disease (SVD) strokes typically involve small areas of infarction and have a better prognosis than LVD strokes.16,22 An SVD stroke can occur when disease develops in the smaller penetrating arteries—usually lipohyalinosis, a degeneration that forms glassy substances which block arteries. Eclampsia and arteritis commonly cause lacunar strokes.

Embolic stroke is the third main ischemic subtype; it results from clots that develop in the heart or elsewhere in the body. Embolic sources include fat emboli related to long bone fractures and particulate emboli due to intravenous drug abuse. The principal sources of cardioembolism are atrial fibrillation, acute myocardial infarction (MI), valve disease, cardiomyopathy, and endocarditis.26 Cardioembolic stroke is often more severe than LVD or SVD stroke.16 Some cardioembolic strokes cause multiple acute infarctions simultaneously.

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