MRI Brain FLAIR, DWI, and SWI

FLAIR

DWI

SWI

Left: FLAIR, Middle: DWI, Right: SWI.

Fluid Attenuated Inversion Recovery (Flair) is similar to a T2-weighted image except it has a long inversion time. This removes signal from the cerebrospinal fluid (CSF) in the resulting images making it appear in black. By doing so, abnormalities on T2 remain bright but normal CSF fluid is attenuated and made dark. This sequence is very sensitive to pathology and makes the differentiation between CSF and an abnormality much easier.

The principle of diffusion-weighted imaging (DWI) is based on how easily water molecules are able to diffuse in a region. The more easily water can diffuse the less initial T2* signal will remain. For example, water within CSF can diffuse very easily, so very little signal remains and the ventricles appear black. In contrast, water within brain parenchyma cannot move as easily due to cell membranes getting in the way and therefore the initial T2* signal of the brain is only somewhat attenuated.

Spontaneous movements of water rapidly become restricted in ischemic brain tissue. During ischemia, the sodium - potassium pump shuts down and sodium accumulates intracellularly. Water then shifts from the extracellular to the intracellular space due to the osmotic gradient. As water movement becomes restricted intracellularly, this results in an extremely bright signal on DWI. Thus, DWI is an extremely sensitive method for detecting acute stroke.

Susceptibility weighted imaging (SWI) is a sequence of MRI that is sensitive to compounds which distort the local magnetic field and it is a velocity corrected gradient-echo MRI sequence. Compounds such as blood or calcium distort the magnetic field and result in loss of signal. Hemorrhage is best detected with SWI.

In the above MRI images, note the infarcted area in the frontoparietal area (MCA) with DWI hyperintensity consistent with restricted diffusivity (water in infarcted area cannot diffuse therefore appears bright on DWI). Notice the hemorrhagic transformation of the infarct on SWI with hypointense signal intensity lesions within the infarcted area.