Cerebrovascular Disease

Cerebrovascular Disease is a topic covered in the Washington Manual of Medical Therapeutics.

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General Principles

  • Stroke is a medical emergency that requires rapid diagnosis and treatment. Remember that “Time Is Brain.”
  • The hallmark of stroke is the abrupt interruption of cerebral blood flow to a specific brain region, resulting in a sudden-onset focal neurologic deficit.
  • Fluctuation of functional deficits after stroke onset or a brief deficit known as TIA suggests tissue at risk for infarction that may be rescued by reestablishing perfusion.

Epidemiology

More than 795,000 strokes occur per year in the United States (one stroke every 40 seconds in the US population), and it is the fourth leading cause of death in the United States (one death every 4 minutes).

Etiology

  • Ischemic stroke can be subclassified into atherothrombotic, embolic, hypoperfusion, or hypercoagulable state (the latter being relatively rare).
    • Atherothrombosis results from reduced flow within an artery or embolism of thrombus into the distal segment of an artery.
      • Atherosclerosis is the most common etiology of thrombus formation in large vessels.
      • Less common etiologies include dissection, fibromuscular dysplasia, moyamoya, and giant cell arteritis.
      • Lipohyalinosis, usually because of hypertension, is the most common etiology of small-vessel disease.
    • Cardioembolic strokes account for about 20% of all ischemic strokes. High-risk cardiac sources include atrial fibrillation, sustained atrial flutter, rheumatic valve disease, atrial or ventricular thrombus, dilated cardiomyopathy, prosthetic valve, bacterial endocarditis, nonbacterial endocarditis (antiphospholipid antibody syndrome, marantic endocarditis, Libman–Sacks endocarditis), sick sinus syndrome, and coronary artery bypass graft surgery.
    • Hypoperfusion occurs because of general circulatory problems and often results in bilateral symptoms. Infarction commonly occurs in border zones between large vessels, resulting in watershed infarcts.
    • Hypercoagulable states may predispose to arterial thrombosis. These include sickle cell disease, polycythemia vera, essential thrombocythemia, thrombotic thrombocytopenic purpura, antiphospholipid antibody syndrome, hyperhomocysteinemia, etc. Factor V Leiden, protein C and S deficiency, and antithrombin (AT)-III deficiency typically result in venous, not arterial, infarcts.
  • Hemorrhagic stroke occurs in about 20% of all cases.
    • The location of an intraparenchymal hemorrhage (IPH) may suggest its etiology.
      • Hemorrhage in the basal ganglia, thalamus, or pons is often because of chronic systemic hypertension.
      • Amyloid angiopathy typically causes lobar hemorrhages and is a common etiology in the elderly.
      • Head trauma, anticoagulants, drugs (cocaine or amphetamines), arteriovenous malformation (AVM), tumor, blood dyscrasia, hemorrhagic conversion of an ischemic stroke, and vasculitis are other possible hemorrhagic stroke etiologies.
    • Aneurysmal subarachnoid hemorrhage (for this section, SAH will refer to aneurysmal subarachnoid hemorrhage unless designated otherwise) is caused by the rupture of an arterial aneurysm resulting in bleeding into the subarachnoid space (which contains CSF). Hypertension, cigarette smoking, genetic factors, and septic emboli (resulting in mycotic aneurysms) can all contribute to aneurysm formation.
  • Cerebral venous sinus thrombosis (CVST) is the occlusion of a venous sinus(es) by a thrombus. It occurs in hypercoagulable states such as late pregnancy or postpartum, cancer, and thrombophilias, as well as with trauma and adjacent inflammation/infection. It may manifest with ischemic infarcts and/or hemorrhage.

Risk Factors

Major significant risk factors for ischemic stroke include hypertension, prior TIA/stroke, carotid stenosis, diabetes mellitus, dyslipidemia, heart failure, cigarette smoking, alcohol consumption, oral contraceptive use, obesity, genetics, and age.

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