 This is another examination of a patient who had known multiple sclerosis and was being evaluated for the effectiveness of therapy. As I stated earlier, I'd like to have up initially the axial flare, the axial T2-weight scan, and the diffusion-weight scan. In this case, on the right-hand side, you're seeing the ADC map that allows us to look for areas of cytotoxic edema without having the issue of T2 shine through. So we can see right from the bat that this patient has a large volume of demyelination. As we scroll through the posterior fossa, initially we're going to let our eyes stray to the T2-weight scan as the most accurate for identifying demyelinating plaque. As I said, the demyelinating plaques are better seen on the T2-weight scan, and it's also because of the prevalence of CSF ghosting artifact that you see on flare imaging. Flare is particularly susceptible to CSF pulsation artifact, and therefore what we're seeing going through the brainstem on the left-hand side is actually CSF ghosting artifact rather than demyelination. It's not seen on the T2-weight scan. Yet another argument for using the T2-weight scan in the posterior fossa. Now if we look at the T2-weight scan at this juncture, we are identifying a central area within the ponds of demyelination, which is quite hard to see here on the flare imaging. Let's continue to scroll further superiorly. Again, we're seeing some areas in the central ponds on the T2-weight scan that I would call areas of demyelination in this patient, but not really reliably seen on the flare imaging. I think I've made my point. As we scroll further superiorly, we come to the supertentorial region. Now we're going to focus a little bit more on the flare imaging going back and forth, and we see that there is a large volume of demyelination in the periventricular regions, as well as in subcortical regions. I generally am not that critical with regard to whether something is subcortical or juxtacortical or deep in the white matter. So for example, here on the flare scan we have the pia, the sulcus, and in this example I would call this a juxtacortical demyelinating plaque. I would call that one as well, juxtacortical. I would call this one juxtacortical. Some people when they're looking at the centrum semio valley in lesions that are not adjacent to the gray matter will use the term deep white matter lesions rather than using it juxtacortical. Why do I bring this up? Why is this important? Well the McDonald criteria specify that the four locations are juxtacortical or subcortical, periventricular, infertentorial, and spinal cord lesions. So if you just had lesions like this that are in the deep white matter without being close to the gray matter, would you include them and say that it does indeed fulfill the criteria of two or more locations, i.e. juxtacortical and periventricular or not? So depending upon what a stickler you are for the nomenclature you may count these as juxtacortical or not. Again as we look at these lesions we're going to be looking both at the ADC map to see whether there is any area of cytotoxic edema as well as the post-gadolinium enhanced scans. Now just looking at these white matter lesions, can I predict which ones are going to show contrast enhancement or not? That's not something that is easily done on T2 or flare scans. You think, ah, this one seems a little different than the other one, so it might show contrast enhancement and be an active plaque. That is very hard to predict and hence we have to do the post-gadolinium enhanced scans certainly for the initial evaluation of the patient. However, the fulfillment of the criteria of being spaced out in time as a polyphasic disorder, a disorder in which there are different aged lesions, one can fulfill that criteria by having a prior study and showing new lesions on flare scan that were not present on the prior study. So the two ways we say that the patient has demyelinated plaques of different ages is by showing whether the plaques are enhancing or not and whether or not they pre-existed on a prior study. So let's eliminate the drama and let's see how the patient looks on the post-gadolinium enhanced scan. Well I'll scroll them together and we'll try to fix that in a moment. So here we have a patient who has multiple enhancing plaques, some of which are showing more of an open arc appearance, some of which are showing a complete rim of enhancement, some of which are showing solid enhancement and I would even say some of which show more of a linear pattern of enhancement. At this juncture we can see that there are some plaques that are enhancing and let's just stop here. These are fairly analogous sections. Here we have the hand knob area and what we're seeing is a plaque here that does not enhance versus multiple other enhancing plaques. So once again here we have a non-enhancing plaque, here we have a non-enhancing plaque, here we have non-enhancing plaques. So these we would say no active blood-brain barrier breakdown and therefore we would assume that these are more chronic as opposed to those that are showing contrast enhancement which are demonstrated also on the flare scan. So spaced out in both location as well as in age, defining it as multiple sclerosis by McDonald criteria. I'd like to pull down the coronal scan just to remind you of the value of scrolling through the orbits to ensure whether or not the patient has active optic neuritis. This is an example of a patient whose optic nerves do not show contrast enhancement. So please utilize all the pulse sequences because to demonstrate the optic nerve demyelination on the axial flare or T2 weighted scan is quite hard. I'm pulling down the sagittal, again the sagittal flare scan very useful. It shows us that the patient has atrophy of the corpus callosum and this is a little bit more ragged in the colosal septal interface, so let me demonstrate that. As opposed to the previous case where I showed a fine linear area of bright signal intensity at the colosal septal interface, this has a more ragged area identifying the demyelination of the at the colosal septal interface and that again is characteristic of multiple sclerosis as opposed to other demyelinating disorders. And you also get a better sense of just how dramatic the demyelination is on the sagittal flare scans. If one were to make a coronal reconstruction from the sagittal scan, you may be able to identify demyelination in the optic nerves. That would be another option. So yet another example of a patient who has pretty robust active multiple sclerosis with both enhancing and non-enhancing plaques, in this case none of which showed cytotoxic edema on the diffusion weighted scan but multiple ones showing contrast enhancement in the brain. On the sagittal flare scan you might also get a chance to look at the cervical spine if that has not been separately scanned. In this case there's nothing dramatic seen in the cervical spine in this patient.