Ischemie

MRI
MRI is more time consuming and less available than CT but has significantly higher sensitivity and specificity in the diagnosis of acute ischemic
infarction in the first few hours after onset.

Early hyperacute
Within minutes of arterial occlusion, diffusion-weighted imaging demonstrates increased DWI signal and reduced ADC values 4,10. This correlates well
with infarct core (for a detailed discussion of DWI and ADC in stroke see diffusion-weighted MRI in acute stroke). At this stage, the affected
parenchyma appears normal on other sequences, although changes in flow will be detected (occlusion on MRA) and the thromboembolism may be
detected (e.g. on SWI). Slow or stagnant flow in vessels may also be detected as a loss of normal flow void and high signal on T2/FLAIR and T1
C+ (intravascular enhancement).

If infarction is incomplete then cortical contrast enhancement may be seen as early as 2 to 4 hours10.

Late hyperacute
Generally, after 6 hours, high T2 signal will be detected, initially more easily seen on FLAIR than conventional fast spin echo T2 10. This change
continues to increase over the next day or two.

T1 hypointensity is only seen after 16 hours 10, and persists.

Acute
During the first week, the infarcted parenchyma continues to demonstrate high DWI signal and low ADC signal, although by the end of the first week
ADC values have started to increase. The infarct remains hyperintense on T2 and FLAIR, with T2 signal progressively increasing during the first 4
days. T1 signal remains low, although some cortical intrinsic high T1 signal may be seen as early as 3 days after infarction 10. After day 5 the cortex
usually demonstrates contrast enhancement on T1 C+10. Less common patterns of enhancement include arterial enhancement, encountered in
approximately half of strokes and becomes evident after 3 days, and meningeal enhancement which is uncommon and is usually seen between 2 and
6 days 10.

Hemorrhage, most easily seen on susceptibility weighted imaging (SWI), is not a good indicator of age. Although most commonly seen after 12 hours
and within the first few days, it may occur earlier or as late as 5 days 10.

Subacute
ADC demonstrates pseudonormalization typically occurring between 10-15 days 10. As ADC values continue to rise, infarcted tissue progressively gets
brighter than normal parenchyma. In contrast, DWI remains elevated due to persistent high T2/FLAIR signal (T2 shine through), unless hemorrhage
(T2 blackout) or cystic encephalomalacia 10. T2 fogging is also encountered typically between 1 and 5 weeks, most commonly around week 2 10,11.

T1 weighted sequences continue to show hypointensity with cortical intrinsic high T1 signal due tocortical laminar necrosis or pseudolaminar
necrosis 10. Cortical enhancement is usually present throughout the subacute period.

Chronic
T1 signal remains low with intrinsic high T1 in the cortex if cortical necrosis is present 10. T2 signal is high. Cortical contrast enhancement usually
persists for 2 to 4 months 10. Importantly if parenchymal enhancement persists for more than 12 weeks the presence of an underlying lesion should be
considered 10.

ADC values are high, resulting in high signal. DWI signal is variable, but as time goes on signal progressively decreases.