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  • Stroke involves abrupt onset of focal neurologic deficit that lasts at least 24 hours and is presumed to be of vascular origin. Stroke can be either ischemic or hemorrhagic. Transient ischemic attacks (TIAs) are focal ischemic neurologic deficits lasting less than 24 hours and usually less than 30 minutes.



  • Ischemic strokes (87% of all strokes) are due either to local thrombus formation or emboli occluding a cerebral artery. Cerebral atherosclerosis is a cause in most cases, but 30% are of unknown etiology. Emboli arise either from intra- or extracranial arteries. Twenty percent of ischemic strokes arise from the heart.

  • Carotid atherosclerotic plaques may rupture, resulting in collagen exposure, platelet aggregation, and thrombus formation. The clot may cause local occlusion or dislodge and travel distally, eventually occluding a cerebral vessel.

  • In cardiogenic embolism, stasis of blood flow in the atria or ventricles leads to formation of local clots that can dislodge and travel through the aorta to the cerebral circulation.

  • Thrombus formation and embolism result in arterial occlusion, decreasing cerebral blood flow and causing ischemia and ultimately infarction distal to the occlusion.


  • Hemorrhagic strokes (13% of strokes) include subarachnoid hemorrhage (SAH) and intracerebral hemorrhage. SAH may result from trauma or rupture of an intracranial aneurysm or arteriovenous malformation (AVM). Intracerebral hemorrhage occurs when a ruptured blood vessel within the brain causes a hematoma.

  • Blood in the brain parenchyma causes mechanical compression of vulnerable tissue and subsequent activation of inflammation and neurotoxins.


  • Patients may be unable to provide a reliable history because of neurologic deficits. Family members or other witnesses may need to provide this information.

  • Symptoms include unilateral weakness, inability to speak, loss of vision, vertigo, or falling. Ischemic stroke is not usually painful, but headache may occur in hemorrhagic stroke.

  • Neurologic deficits on physical examination depend on the brain area involved. Hemi- or monoparesis and hemisensory deficits are common. Patients with posterior circulation involvement may have vertigo and diplopia. Anterior circulation strokes commonly result in aphasia. Patients may experience dysarthria, visual field defects, and altered levels of consciousness.


  • Laboratory tests for hypercoagulable states should be done only when the cause cannot be determined based on presence of risk factors. Protein C, protein S, and antithrombin III are best measured in steady state rather than in the acute stage. Antiphospholipid antibodies are of higher yield but should be reserved for patients younger than 50 years and those who have had multiple venous or arterial thrombotic events or livedo reticularis.

  • Computed tomography (CT) and magnetic resonance imaging (MRI) head scans can reveal areas of hemorrhage and infarction.

  • Carotid Doppler (CD), electrocardiogram (ECG), transthoracic echocardiogram (TTE), and transcranial Doppler (TCD) studies can each provide valuable diagnostic information.

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