Health Questions and Answers


What is a stroke?
A stroke is focal brain dysfunction due to ischemia. The ischemia may arise from atherosclerotic narrowing of a blood vessel, an embolus, hemorrhage, or other causes.

Distinguish among the four main kinds of stroke.

Type % of All Strokes Onset Preceding TIAs (%) Altered Mental Status (%) MRI or CT Scan Other Features
Thrombotic 40 May be gradual Up to 50 5 Ischemic infarction Carotid bruit Stroke during sleep
Embolic 30 Sudden 10 1 Underlying heart disease, peripheral emboli, or strokes in different vascular territories. row 2, cell 7
Lacunar 20 May be gradual 30 0 Small, deep infarction Pure motor or pure sensory stroke
Hemorrhagic 10 Sudden 5 25 Hyperdense mass Nausea and vomiting, decreased mental status

What are the clinical features of a thrombotic stroke?
Thrombotic strokes are the most common type and account for approximately 40% of all strokes. They may have a gradual, stuttering, or stepwise onset rather than an abrupt deficit. The cause is generally atherosclerosis affecting large intracranial vessels. The large-vessel involvement explains why these strokes tend to cause considerable neurologic deficit. About one-third to one-half of thrombotic strokes are preceded by transient ischemic attacks (TIAs), which are focal but totally reversible deficits that last a few minutes.

Describe the major clinical features of an embolic stroke.
Embolic strokes generally arise from the heart with an underlying cardiac disease, such as atrial arrhythmias, valvular disease, or mural thrombus. They tend to be abrupt in onset, with more rapid resolution, and tend to cause smaller neurologic deficits than a thrombotic stroke. Because the embolus travels in the arterial stream until it reaches a blood vessel of sufficiently small caliber to occlude it, it often travels distally all the way to the cortex. Cortical deficits, such as aphasia, are thus characteristic of embolic strokes.

Explain the mechanisms of a lacunar stroke.
Lacunar strokes are very small, discrete infarcts, < 1 cm3 in size, occurring deep within the brain or brain stem (lacune means little lake or pond). These strokes are due to occlusion of tiny penetrating arterioles that supply the deep brain substance, usually in the region of the basal ganglia, thalamus, and internal capsule, as well as the brain stem. These small strokes may cause discrete clinical symptoms, such as a pure motor stroke (hemiparesis without sensory loss) or pure sensory stroke.

How do hemorrhagic strokes differ from the other three types?
An intracerebral hemorrhage is classified as a stroke because of its abrupt onset with focal neurologic deficits, but it is due to rupture of a blood vessel, with subsequent bleeding and intracerebral mass, rather than to ischemia directly. Intracerebral bleeds have an abrupt onset and are usually accompanied by a significant headache and other signs of increased intracranial pressure, such as nausea, vomiting, and a diminished mental status. These are often devastating events with a poor prognosis. Bleeds tend to occur in the same deep locations as lacunae (i.e., the basal ganglia and brain stem).

What are the leading causes of death shortly after a stroke?
The three leading causes of death in the first 30 days after a stroke are not related primarily to the stroke itself or to neurologic deficits:

  1. Pneumonia
  2. Pulmonary embolus
  3. Ischemic heart disease

Discuss the medical management of the patient with acute stroke.
Medical management of the stroke patient should focus on the complications that develop after the stroke. Since the leading cause of death is pneumonia, care should be taken that the patient does not aspirate-keep the patient NPO until it is clear that swallowing is not impaired by neurologic damage. Fever should always be presumed to be pneumonia until proved otherwise. Measures to prevent pulmonary embolus should be instituted, including early mobilization. Ischemic heart disease commonly causes death, since atherosclerosis affecting the cerebral vasculature probably also involves the coronary arteries. Cardiac assessment should be individualized.

When should thrombolysis be used to treat acute ischemic strokes?
Recombined tissue plasminogen activator (TPA) is approved for the acute treatment of ischemic stroke, but only in certain settings. It must be given as soon as possible after the stroke and certainly within the first 3 hours. A CT scan of the head must not show any evidence of infarction (i.e., tissue damage must not be severe or hemorrhage). The patient must have significant deficits (the drug should not be used if the patient will recover well without it), and there should be no other contraindications, such as active bleeding or severe hypertension. Few patients, in fact, meet all these requirements and are candidates for TPA.

How is thrombolytic therapy given?
Patients are treated with 0.9 mg/kg TPA given over 1 hour after an initial 10% bolus. Studies suggest that such patients show approximately 30% more recovery of function than untreated patients. The risk of intracranial hemorrhage is approximately 6%; patients should be carefully monitored.

When is anticoagulation indicated in cerebrovascular disease?
The role of anticoagulation in cerebrovascular disease is highly controversial. The consensus among neurologists is that anticoagulation is mainly of benefit to prevent embolic stroke from the heart. Following an initial brain embolus from a cardiac source, the risk of subsequent emboli is high, especially within the first few days and weeks, and evidence suggests that immediate anticoagulation reduces the risk. Although there is a chance that anticoagulation will worsen a stroke by converting the ischemia into hemorrhage, data suggest that this worsening is more than outweighed by the benefits in preventing further emboli.

Discuss the role of aspirin in the management of cerebrovascular diseases.
Aspirin, given at the time of a stroke, may have some protective effects. Patients with TIA or minor stroke are often treated with aspirin, usually 1 tablet (325 mg) per day, to prevent further episodes of cerebrovascular ischemia. There may be additional benefits to combining aspirin with dipyridamole.

What is the role of ticlopidine and clopidogrel in the management of cerebrovascular disease?
Ticlopidine, like aspirin, acts as a platelet inhibitor and similarly decreases the risk of further cerebrovascular ischemia. Unlike aspirin, it does not affect the cyclo-oxygenase pathway and instead acts by interfering with platelet membrane interactions. Clopidogrel is another antiplatelet agent with similar properties. Their current role is primarily for the prevention of stroke in patients with cerebral ischemia for whom aspirin therapy has failed, has caused intolerable side effects, or is otherwise contraindicated.

What is the main indication for carotid endarterectomy in cerebrovascular disease?
For patients with symptomatic atherosclerotic stenosis of > 70% in the carotid artery, carotid endarterectomy is clearly beneficial, significantly decreasing the risk of ipsilateral stroke.

Discuss the role of carotid endarterectomy in asymptomatic patients.
In asymptomatic patients with atherosclerotic stenosis of the carotids, the role of carotid endarterectomy is less clear. Three large randomized trials done in the early 1990s detected no benefit of endarterectomy in these patients. However, the Asymptomatic Carotid Atherosclerosis Study (ACAS) demonstrated a reduction in cerebral infarction in asymptomatic patients with as little as 60% stenosis, provided perioperative morbidity was kept to a minimum. The benefits were sufficiently modest that not all experts were convinced of the utility of surgery, and considerable individual variation remains among physicians managing such patients. Clearly, any surgical intervention in the treatment of carotid artery stenosis must be used in addition to, not in lieu of, aggressive control of modifiable risk factors.

WEB SITES (American Academy of Neurology)


  • Halley EC: Thrombolysis in the treatment of acute ischemic stroke. Curr Treat Opt Neurol 5: 377-380, 2003.
  • Brott T, Bogousslavsky J: Treatment of acute ischemic stroke. N Engl J Med 343:710-722, 2000.
  • North American Symptomatic Carotid Endarterectomy Trial Collaborators: Benefit of carotid endarterectomy in patients with symptomatic moderate or severe stenosis. N Engl J Med 339: 1415-1425, 1998.
  • Aminoff M: Neurology and General Medicine, 3rd ed. Philadelphia, Churchill-Livingstone, 2001.
  • Noseworthy JH (ed): Neurologic Therapeutics. London, Martin Dunitz, 2003.
  • Bradley WG, Daroff RB, Fenichel GM, Jankovic J: Neurology in Clinical Practice, 4th ed. Philadelphia, Butterworth-Heinemann, 2004.
  • Caplan LR: Stroke: A Clinical Approach, 3rd ed. New York, Butterworth-Heinemann, 2000.
  • Samuels MA, Feske S (eds): Office Practice of Neurology, 2nd ed. Boston, Churchill-Livingstone, 2003.
  • Johnson RT, Griffin JW: Current Therapy in Neurologic Disease, 6th ed. St. Louis, Mosby, 2002.
  • Victor M, Ropper AH: Prinicples of Neurology, 7th ed. New York, McGraw-Hill, 2001.

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