Black Holes

[MyGirlsMom]

Hello everyone!

I am looking to learn more about black holes on the MRI and peoples experience and understanding about black holes. It seems that I have black holes and that it is an indicator of more damage from lesions than just the plaque.

Has anyone had black holes in their history and then have had more, new ones? Do black holes get bigger over time? Do people that progress typically have black holes vs lesions?

Thanks for any experiences, knowledge and opinions you can share.

[KoKo]

Hi MyGirlsMom

I have black hole lesions also - areas of permanent damage indicating loss of myelin, and loss of nerve fibers.

You may be interested in this article, which appeared in the National MS Society's magazine (formerly called Inside MS, and now called Momentum).

It's called Bright Spots & Black Holes.

http://findarticles.com/p/articles/m...0/ai_94040948/

Take care,
KoKo

[lemstar]

I have had MS for 31 years, and was only diagnosed two years ago. At that time, they saw black holes. My symptoms are mostly sensory, and so far, my MS has not progressed severely, i.e. I am still walking and working. So black holes are areas that cannot repair themselves, but they are not a death sentence....

[MyGirlsMom]

Thank you both for your response. I did go and read the article you mentioned.

My thought is that at recent neuro visit the disucssion centered around that went I get lesions, they tend to be significant as I end up with black holes. Because an exaserbation results in such significant damage, the goal is to limit the potential for a reoccurance as much as possible. Thus, perhaps Tysabri instead of Copaxone.

Any thoughts?

[KoKo]

MyGirlsMom

My thought is that at recent neuro visit the disucssion centered around that went I get lesions, they tend to be significant as I end up with black holes. Because an exaserbation results in such significant damage, the goal is to limit the potential for a reoccurance as much as possible. Thus, perhaps Tysabri instead of Copaxone.

I am not knowledgeable about the effectiveness or differences with the various DMD's, as I don't use them (PPMS).

But it seems to me that if, after time, a particular DMD isn't lessening the relapses, then a different one would be used.

Maybe if you ask this in the Medications forum too, you may get some good feedback?

Take care,
KoKo

[0485c10]

I had a persistent black hole when i was diagnosed. the doc didn't tell me about it i found out it was there when i got a copy of my cd...it was in the frontal lobe and it was the largest of my distinct lesion. i have small lesions and confluent lesions...

it caused me to investigate & book mark things about black hole. i will put links to all of the sites i found. your gonna find more i'm certain.

i did read the pharmaceutical companies had defined bh, what constituded a bh, in order to report drug effectivenes. i said i had a persistant bh, it never become a chronic bh..drug companies will report the effectiveness of their drugs by how many pesistant bh did not become chronic while using their med.

Active BH = a dark(hypointense) lesion on a t1 mri scan without dye. if dye had been used the lesion would have enhanced. so an active black hole is just an active lesion..

Persistant BH= a dark (hypointense) lesion on a t1 mrii with the dye.

Chronic BH = a Persistant BH that has remained for at least 6 months and is thought to be permenant.

I had a Pesistant BH that never become perminant. and no more since.

i believe i read at the time, maybe it was in the nih database? it was more than 5 years ago that i read it. It said that the tendancy to develop black holes is thought to be genetic or something like that. individual in a person. some people will develop many and other not at all. that jives with what they told you at the doc office that your lesions tend to cause more tissue damage of bh.

i'm pretty sure i read that one theory is its a genetic tendency in some people. i will look around and see if i can find it, but it was many years ago i read something like that? Nothing in MS is absolute, so i'm sure that 5 years ago i read that it was a theory.

instead i will leave you links to articles and pictures i have book marked on bh.


http://www.medhelp.org/health_pages/...show/23?cid=36

http://www.ajnr.org/cgi/content/full/20/5/813/F2

http://www.ajnr.org/cgi/content/full/28/10/1843/F5


And tysabri is doing well for me, i would not hesitate in your decision to go from copaxone to tysabri.

that first article describes how bh go to atrophy. some brain tissue can be lost without affecting function(about 40% if i remember what i read, correctly???? again it was about 5-7 years ago), but you certainly do not want to lose brain tissue if you don't have to. switch to tysabri imo. good luck.

[0485c10]

Here is a clinical trial for betaseron Benefit trial & if you go down secondary outcome measures of the trial it says...

MRI-based Efficiency domain: Absolute change in volume of bh from screening MRI to month 60.

Absolute change of volume of black holes from screening MRI to month 60 was calculated as volume of black holes at month 60 minus volume of black holes at screening.

http://clinicaltrials.gov/ct2/show/NCT00185211

this is still not the article i remember about some people will create more bh & it was thought to be genetic.

bummer i wish i knew where that article was.

[0485c10]

Here is a trial report, i think, that reports the conversion from Acute BH to Chronic BH was lower in betaseron(15.2%) than Copaxone (21.4%)

(ABH)Acute BH = (NEL) Newly Enhancing Lesion

as i defined in a previous response...definitions of type of bh.

the majority of ABH do not develop CBH from ABH, but about a quarter did.

see these black hole definitions were driven by pharmaceutical trial reports.

http://www.ncbi.nlm.nih.gov/pubmed/19687024

and in this article it found that BH were higher in SP & PP than in RR. Higher in male PP than female PP.

and greater in age of onset for RR?...but it does not tell if its a higher age of onset or a lower? but it does say its higher for a greater disease duration....so onset at a younger ages gives the possibility off a larger disease duration than an older age of onset??

i wish they would write their abstracts with more details

http://www.ncbi.nlm.nih.gov/pubmed/11176939


Ah huh--gold mine!!!!
this is the one where it mentions genetic factors. lots of good stuff in this article. i think this is the one i found 5 years ago....

In the 2nd paragraph under introduction it says.....

this suggest some patients may be genetically prone to bh--a combination of unknown genetic factors & the frequency of bbb disruptions has been shown to correlate
with an earlier age of onset in RR or SP.

i'm just skimming this fast as i type it, i do not gaurentee i have written correctly what it said. I did leave a link for you to check it your self , don't trust what i wrote!!!
its 2 am, past my bed time.

[0485c10]

And this book can be read on line and it has a whole chapter on BH.

Chapter 4 T1 Hypointense Lesions(Black Holes)

http://www.scribd.com/doc/8817608/MR...-of-MS-Lesions'


MRI Atlas of MS Lesions
Sahraian,M.A.;Radue,E-W
2008,XIV,178 p. 218 illus, 9 in color with CD-ROM
Hardcover
ISBN:978-3-540-71371-5


can buy it used at amizon comes with a CD of MRI's showing BH & other lesions.
about $90 used.


http://www.amazon.com/s/ref=nb_sb_noss?url=search-alias%3Dstripbooks&field-keywords=MRI+Atlas+of+MS+Lesions&x=0&y=0

[0485c10]

Forgot to post the link to the "gold mine" article where it mentions genetic factors & younger age of SS SP onset for bh.
(it was 2 am)

http://archneur.ama-assn.org/cgi/content/full/58/1/76