A physician-validated, board-style question from the Active Transport QBank. Try it, then check the reasoning for every option.
A 64-year-old woman is brought to the emergency department 30 minutes after the onset of right-sided weakness and impaired speech. On admission, she is diagnosed with thrombotic stroke and treatment with alteplase is begun. Neurologic examination four weeks later shows residual right hemiparesis. A CT scan of the head shows hypoattenuation in the territory of the left middle cerebral artery. Which of the following processes best explains this finding?
-
A
Gangrenous necrosisIncorrect. Gangrenous necrosis occurs in distal limb/GI ischemia, often with superimposed infection (wet gangrene). It's not a CNS pattern.
-
B
Liquefactive necrosisCorrect. CNS ischemic injury characteristically produces liquefactive necrosis with cyst cavity formation due to enzymatic digestion by microglia and macrophages.
-
C
Caseous necrosisIncorrect. Caseous necrosis is the pattern of granulomatous inflammation (tuberculosis, certain fungi); it's not typical of an arterial thrombotic infarct.
-
D
Fat necrosisIncorrect. Fat necrosis occurs in pancreatitis (saponification) or breast trauma — neither applies to a brain infarct.
-
E
Coagulative necrosisIncorrect. Coagulative necrosis is the pattern of ischemic infarction in most solid organs (heart, kidney, spleen), but the brain is the notable exception — CNS infarcts undergo liquefactive necrosis due to high lipid content and microglial enzymatic digestion.
↑ Tap an answer to reveal the reasoning
Answer: B. A 64-year-old woman had an ischemic (thrombotic) stroke in the left MCA territory four weeks ago. CT now shows hypoattenuation — a hypodense, well-demarcated region representing cystic cavitation of the infarcted brain tissue. The cellular process that produces this is liquefactive necrosis.
The CNS is uniquely susceptible to liquefactive necrosis because: (1) the brain has high lipid content, which liquefies when tissue is destroyed; (2) microglia rapidly migrate to ischemic tissue and release proteolytic and lipolytic enzymes that digest the dead neurons, glia, and myelin; (3) the resulting debris is removed by macrophages, leaving a fluid-filled cystic cavity by 1–3 weeks. By 4 weeks, the well-formed cyst appears hypoattenuated on CT.
Key pearl: every other organ undergoes coagulative necrosis after ischemic injury (heart, kidney, liver, spleen) — but the brain liquefies. The exception within the brain is granulomatous infection like TB, which causes caseous necrosis. Bacterial brain abscesses also cause liquefactive necrosis but with neutrophil infiltration and ring enhancement on imaging.
**Why each option:**
**A.** Gangrenous necrosis occurs in distal limb/GI ischemia, often with superimposed infection (wet gangrene). It's not a CNS pattern.
**B.** Correct — CNS ischemic injury characteristically produces liquefactive necrosis with cyst cavity formation due to enzymatic digestion by microglia and macrophages.
**C.** Caseous necrosis is the pattern of granulomatous inflammation (tuberculosis, certain fungi); it's not typical of an arterial thrombotic infarct.
**D.** Fat necrosis occurs in pancreatitis (saponification) or breast trauma — neither applies to a brain infarct.