Cerebral Ischemia and Hypertensive Changes

Increased risk of disease with diabetes, hypertension, smoking, family history, and hyperlipidemia

Accounts for 70% to 80% of all “strokes”

More common in men than in women

Increased incidence with age—1/1000 for ages 45 to 55 years, 1/33 over 85 years of age

Prognosis is dependent on severity of ischemic event

Immediate thrombolytic therapy can improve outcomes

Preventative therapy includes aspirin, antiplatelet medications, treatment of hypertension and diabetes, smoking cessation, and lowering of cholesterol

After 1 to 2 days, wedge-shaped lesion of hypodensity on CT and T1-weighted MRI in classic cerebrovascular distributions of blood supply

Diffusion weighted MRI can detect changes within minutes of ischemia

6 to 8 hours of infarction—no detectable findings

First noticeable change is subtle blurring of gray-white junction

24 to 48 hours postinfarction—brain swelling, hyperemia, and dusky discoloration in a well-defined vascular territory

Large infarcts lead to mass effect with possible herniations

Embolic infarcts with reperfusion lead to hemorrhagic areas of necrosis

No microscopic changes within 12 hours of event

12 to 48 hours: circumscribed areas of pallor with “red-dead neurons” (cytoplasmic hypereosinophilia on H&E stain and shrunken, pyknotic nuclei)

3 to 30 days (subacute phase) consists of macrophage infiltrate with cavitation of cortical layers two to six and loss of axons within lesion

Months to years: remote infarction typically consists of circumscribed organized area of cavitation with scattered macrophages and residual glial tissue

Typically not necessary

Primary brain hemorrhage

Glioma (may mimic early stages of infarction on imaging)

Active demyelination