1. FLAIR and T2

2. Diffusion sequence will have 3 sets of images often fused in a series and will include B0, B500, and B1000

3. Diffusion and ADC

4. What information does the Facility need?
Is the infarct acute, subacute, or chronic
What structures are involved (cortex, basal ganglia, thalamus, brainstem)
Size of infarction small, medium, large (always also give actual measurement in cm)
Describe complications (mass effect on ventricles, herniation, hemorrhagic blood products, area of potential penumbra)
Don’t forget the Circle of Willis

5. Favoring a Chronic Infarct
Ex vacuo dilation of adjacent ventricle
Encephalomalacia
Use prior studies
Hyperintense on ADC
Laminar Necrosis

6. Laminar Necrosis
Will show cortical T1 curvilinear hyperintense signal which becomes evident after 2 weeks, peak at 1 to 3 months, and will slowly but still be visible for months to years.
The high T1 signal is  caused by the accumulation of denatured proteins in dying cells and Does Not represent presence of hemorrhage.

7. Old Infarct
Diffusion ADC T1

8. Differentials that appear bright on diffusion
Infarction
Epidermoid Tumor
Bacterial Abscess
Acute Demylination
Tumor with high nuclear/cytoplasmic ratio
Acute Encephalitis
T2 Shine through
Subacute Blood or high protein content
Jacob Creutzfeld Disease

9. Infarction Timing Acute (hours-7 days)
CT, T1, and T2 changes may not be apparent for up to 6 hours.
Restricted diffusion and decreased ADC value is seen within minutes of onset with peak black ADC occurring 1-4 days.
Subacute (1-3 weeks)
ADC shows pseudo normalization to isointense peaking in 2nd week
Continued restricted hyperintensity on Diffusion
Chronic
Diffusion becomes low signal to mildly hyperintense as T2
ADC becomes hyperintense