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572651 tn?1530999357

? from CanCanRun - black holes

Our new member CanCan posted this on a very old, long thread and I think it deserves some attention separately.  Please jump in with your knowledge of Black holes..........


Anyone have any idea how radiologists differentiate between a "black hole" lesion in an MRI and something else?  I just got a brain MRI last week and the radiologist noted that the lesion on my frontal lobe is unchanged since last MRI... and there are several "punctate foci of hyperintensity in the inferior right frontal lobe" - which, in his opinion, is a "perivascular space" issue.  

I have a black hole lesion on my c-spine, so I know they show up dark in T1 and bright in T2 MRIs, which is exactly how these "foci" are presenting. I even found them in my MRI, before getting the results, because they stood out so much. They are clustered, and directly adjacent to my ventricle, which as I understand it, is a common feature of MS lesions.  I'm not saying these are, in fact, MS lesions, but am curious as to how radiologists tell the difference - and if it really is a judgement call.
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572651 tn?1530999357
I'm glad that was of use to you - Quix has left us some wonderful material to use.  Kwarendorf, I know that church nod all too well, thanks for giving it a name.  LOL
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1831849 tn?1383228392
I am the proud owner of a black hole. Every time I start to read about what this means my eyes start to glaze over and the church nods start. I guess this black hole topic has fallen into the category of things I'm not meant to understand :-)
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1045086 tn?1332126422
I had come across that post by Quix not too long ago.  As always, she says it best - in a way we can understand.  What a mind!

I'm with you JJ about looking at those MRIs.  I loved it when you concluded, "knowing why that black spot shouldn't be there and the other ones should, takes more training than any of us lay people have."  We learn a lot here but it's tough to catch up on an entire medical education with online study no matter how many hours we spend gazing at white spots and black dots.

As for wanting to be educated and informed about MS?  Good for you CCR!!  Strong self advocacy is essential for PwMS.  You go girl :)
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987762 tn?1671273328
COMMUNITY LEADER
Hi and welcome,

I think its almost impossible for the untrained eye to determin the complexities in our MRI's, things like black holes are definitely really difficult to work out. I've even looked at the many MRI's you can find online, i stick mainly to the reputable research and MS organisations and still the ones that they identify as a black hole, (with nice helpful little arrows or within a circular coloured pen mark) and still i'm ok ummmm, yeah sure i see it, errrr not! lol

These identified black holes often look the same as other dark splotches or spots, so knowing why that black spot shouldn't be there and the other ones should, takes more training than any of us lay people have. You'll see what i mean if you have a look at what MS Australia Research says about black holes.

http://www.msra.org.au/next-20-article-black-hole-ms

I do know when i was looking at the lesions on my T1 scans, there are a couple of ovalish black spots, that to my untrained eye looked just as wrong as the numerous white ovals on my T2's but if they are true black holes i couldn't say because they were not reported. So with out asking the neuro or technicaian, i can only speculate and wonder if that little circular blackness in my cerebellum is meaningful or not.

"In spite of their potential role as a surrogate in MS, there is relatively little literature on objective identification and quantification of black holes. "

see http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1808226/  

So after trying to find you something relivant (as above) all i'm left with is another question, do they actually look for black holes?

cheers........JJ
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Avatar universal
Thanks so much, Lulu, for passing this along.  It would be great to get some more insight if anyone knows much about this subject.

I really wish there was a course that we could sign up for that would walk us through all of these questions, and give us a thorough understanding of the disease that we will spend the rest of our lives battling. Our doctors just don't have the time to sit down with us each individually and explain all of these things in detail - so we're left wondering and then searching for answers when we stumble upon something we're unfamiliar with (which seems to be fairly often for me). I have learned more about the brain anatomy and MRIs in the past few days than I did in my entire life up to this point!  I know people with MS who don't even care to look at their MRIs, but I want to be educated and informed about them - it is MY body after all. =)
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572651 tn?1530999357
and don't miss the health page written by shoshin -

http://www.medhelp.org/health_pages/Multiple-Sclerosis/Neurodegeneration-in-MS/show/716?cid=36

Lots of great information from both of these wise women.
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572651 tn?1530999357
I found this thread from 2010 about black holes and a great explanation from Quix -
http://www.medhelp.org/posts/Multiple-Sclerosis/mostly-neuron-death/show/1250913

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.

http://www.medhelp.org/health_pages/Multiple-Sclerosis/Lesions-Lesions-Lesions/show/762?cid=36

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.

Quix
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