CT in acute ischemic stroke

Hyperacute phase: 0-24 hours

  • Early hyperacute phase: 0-6 hours. Late hyperacute phase: 6-24 hours
  • A hyperdense vessel may be the only finding on unenhanced brain CT in the early hyperacute phase
  • Loss of grey-white matter differentiation
  • Hypoattenuation and “disappearance” of deep nuclei
  • Hypoattenuation of cortex and parenchymal swelling results in gyral effacement (eg “insular ribbon” sign)
  • CTA may reveal vessel occlusion, dissection or thrombosis
  • Perfusion CT evaluates the cerebral blood flow CBF, the cerebral blood volumeCBV and the mean transit time MTT. These three parameters are related as follows:
    1. All ischemic tissue will show reduced MTT
    2. The irreversibly injured infarct core will show reduction in both CBF and CBV
    3. The potentialy salvable ischemic penumbra will show mismatch between reduced CBF but normal or even transiently increased CBV
    4. 15-20% of large MCA infarcts will show reduced CBF in the contralateral cerebellum (crossed cerebellar diaschisis)
  • The CT hyperdense MCA sign should not be used as a criterion to withhold IV alteplase from patients who otherwise qualify.
  • Multimodal CT and MRI, including perfusion imaging, should not delay administration of IV alteplase
  • It may be reasonable to incorporate collateral flow status into clinical decision making in some candidates to determine eligibility for mechanical thrombectomy.

Acute phase: 24 hours - 1 week

  • Hypoattenuation and development of cytotoxic edema become more marked
  • Mass effect from the edema may result in parenchymal herniation or vessel compromise and further infarct development
  • Ischemic vascular damage may result in hemorrhagic transformation in 20-25% of cases
  • When CTA has been performed, contrast extravasation caused by a disrupted blood brain barrier may mimic hemorrhagic transformation. Dual-energy CT scanning helps in differentiating the two.
  • Patchy enhancement may be seen on contrast-enhanced CT. It appears ~2 days after onset, peaks at 2 weeks and disappears by 2 months (“2-2-2 rule”)

Subacute phase: 1-3 weeks

  • The edema starts to subside 7-10 days after stroke onset
  • Cortical or deep grey substance small petechial hemorrhages (not to be confused with hemorrhagic transformation) may develop which increase the attenuation and contribute to the ”fogging phenomenon”
  • Fogging phenomenon is the appearance of infarcted grey matter as normal or near normal on non-enhanced CT usually performed in the subacute phase of the infarct. Factors that may contribute to this phenomenon include:
    1. Migration of lipid-laden macrophages into the infarcted tissue
    2. Decrease in edema
    3. Development of small petechial hemorrhages
    4. Capillary proliferation If this presents a diagnostic problem, an MRI scan or contrast-enhanced CT will promptly demarcate the infarcted region.

Chronic phase: >3 weeks

  • Sharp demarcation of infarcted area
  • Dystrophic calcification may occur
  • Secondary atrophy in the affected hemisphere or contralateral cerebellum
  • Wallerian degeneration may result in volume loss in the ipsilateral cerebral peduncle.
  • Infarcts older than 2 weeks should not enhance on contrast-enhanced CT scans