I found this thread from 2010 about black holes and a great explanation from Quix -
A little background on the topic. First, there is no official "typing" of MS into inflammatory and direct neuronal death. But, we all get lulled into thinking that our MS is made up of the T2 Hyperintense Lesions and that is as far as it goes. Still, most of us know that there is more to MS than the lesions we talk about all the time and there is.
In the Health Page "Lesions! Lesions! Lesions!" we talk about the different types of abnoramlities we see in the MS brain in an MRI. The most common are the T2 Hyperintense ones, but there are also "T1 Black Holes", there are the abnormalities seen in the Normal-Appearing White Matter (NAWM) and there are lesions in the gray matter, the cortex. How all of these play together in MS is still largely a mystery, but we do know that the worst of what happens to us is NOT in the common T2 lesions - the ones we talk about all the time.
The T2 lesions are the ones that are most directly related to the autoimmune inflammatory action of our disease. Those lesions are where the antibodies directed against myelin play their greatest role. Those lesions are also most directly correlated with the relapses of Relapsing Remitting form of MS. It is not a complete correlation, but it is a strong one. More T2 lesions -> generally more relapses and vice versa. It's why the neuros often will do an MRI at the sign of a big relapse - so they can find a new and maybe enhancing lesion. The lesions enhance because the immune attack on the myelin causes inflammation and the inflammation causes a breach in the Blood Brain Barrier. That breach is what allows the contrast material to appear in the brain matter.
But, we all also know that there is another force at work in MS and that is a steady accumulation of disability. For some time the experts in MS have been aware that the progression of disability was not particularly linked to the number of relapses nor to the accumulation of new T2 lesions. So, clearly something else is causing brain damage beyond the antibody attacks on the myelin. A process called direct neuronal (or axonal) degeneration (or death) happens also.
Whereas the T2 lesions are known to be able to repair themselves (to an extent), the damage caused by neuron death is not reversible. The entire nerve cell dies along with the long nerve fiber extending from it, called the axon. One by one as these nerves die, brain tissue is lost and the end result is a shrinking of the total amount of brain tissue. This is called brain "atrophy". Places where there have been a large number of cells that have died can be seen on the MRIs. They are best seen on the T1-weighted technique. They are called "Balck Holes." My understanding is that the black holes are areas of lost brain tissue.
This is a fuzzy area, because some researchers claim black holes can heal and disappear. Hmmm. I don't see how, so I don't totally understand this whole topic. Some people speak about black holes as areas where the brain has lost tissue density and that is how I understand it.
Now, as the typical person with MS goes through life, they have their relapses now and then. Symptoms appear, cause problems, and mostly disappear. But, in the background we see a process of disability occuring - function is lost and not regained. Statisically they can tell that this disability is happening independently of the relapses.
The disability that a person has is far more closely associated with the Black Holes than with the T2 Lesions. This makes sense. On the forum here we have seen many people with tons of T2 lesions, but not much disability. But then, there are other people (like me) with a piddly amount of small lesions, an a lot of disability.
Relapses correlate mostly with T2 lesions.
Disability correlates best with Direct Neuronal Death and with brain atrophy.
In the four types of MS, the largest group is RRMS and their course is mapped by the T2 lesions. The meds for MS target the inflammatory part of the disease course, called the Immuno-Inflammatory lesions which are the T2 lesions we talk about with MRI reports.
The smallest group is PPMS - They have some inflammatory activity, but by far most of their brain damage is in Direct Neuronal Death (Direct Axonal Death). So, the meds which only target the inflammation don't have much affect on them. That is why all of the therapies we have to date don't have much affect. We don't yet know what the "trigger" or cause of this direct tissue death is, so we can't target it yet.
Okay, that part is pretty clear. What did I mean, then, when I said I have RRMS and my neuro said most of my damage is in direct neuronal death? I haven't pinned him down yet on this. I think he is saying that - by all measurements I do not have PPMS. I don't have the proper type of lesions and my pattern of disability is not characteristic of PPMS. Specifically I only have a few lesions at all. And my disability is a persistent and progressive hemiparesis (the right half my body is affected). My neuro said that almost exclusively, eleven years into the disease course (as I am), a person with PPMS will have BOTH legs involved in a spastic paraparesis. (weak lower half of the body). I have only the right leg involved.
So, what can that mean? From all my reading and study of MS it is clear that MS has an almost infinite way of presenting. I think that my picture is one with very few T2 Lesions - and thus little immuno-inflammatory activity. I would likely be in that group of people who does not respond to a DMD. Remember - one of the criticisms against the DMD's is that only about 40% of the people will have a good response to them. They still don't know why the other 60% don't respond. Perhaps they have - on average - a higher amount of progressive disability than the other group.
What this says is that RRMS is hot really a homogenous group. Well, if you have read much on the forum, that is pretty obvious.
This is what I have surmised, and it makes sense to me. But, I have only figured this out and not read it as science. Still, my track record on such things, like my statements more than a year ago that MS frequently DOES affect the Autonomic Nervous System, is pretty good.
Secretly I believe that I will eventually be categorized as PPMS, so all of this might be mute. On the other hand I do have what could be called relapses.
I hope that this clarifies some of the thinking.