FLAIR and T2

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

Diffusion and ADC

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

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

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.

Old Infarct Diffusion ADC T1

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

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