This Is MS Multiple Sclerosis Community: Knowledge & Support

We report a case of moyamoya disease in a young adult female, in whom the initial clinical and radiological features were considered to be compatible with multiple sclerosis. Magnetic resonance imaging (MRI) features of dilated collateral arteries were then recognized, and the initial MRI findings considered to represent demyelination were reinterpreted as areas of infarction. Although rare, moyamoya disease should be considered in the differential diagnosis in young patients presenting with symptoms and signs suggestive of multiple sclerosis. The diagnosis may be suggested by typical MRI findings.

We believe that moyamoya disease should be considered in multiple sclerosis variants who present with paresthesias and do not respond to traditional immunosuppressive therapies.

Early diagnosis and revascularization procedures could help prevent further neurologic sequelae. Furthermore, subtle MRI findings should suggest obtaining a CTA/MRA or a formal angiogram to identify moyamoya vessels

thanks for linking the study over here, Cece. I find it less annoying (for myself) and less confusing to readers to write on Facebook, and appreciate you dealing with TIMS....
cheer

What's most interesting is that it is ischemic injury which activates the immune system and creates lesions in moyamoya disease....which is why it's a differential for MS.


http://www.ncbi.nlm.nih.gov/pubmed/2394073

Again, same MRI demyelination we see in stroke, cerebrovascular disease, and CCSVI. In this instance, it's slowed blood flow going into the brain, and opening the affected intracerebral arteries brings relief.



thanks for linking the study over here, Cece. I find it less annoying (for myself) and less confusing to readers to write on Facebook, and appreciate you dealing with TIMS....
cheer

Here's a great paper explaining the different catagories of demylinating lesions. Moyamoya would be in the ischemic demylinating diseases, along with carbon monoxide poisoning, vasculitis and cerebrovascular disease.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1860500/
cheer

What would the pathological definition of MS be? My understanding is that, as a disease of exclusion, there is no exact way to diagnose MS.

I would say that defining MS by the presence of T-cells mediated diffused demyelinating lesions would be a good approach for a definition.

Here is a study where the CSF of patients with cerebrovascular disease is tested. And those with MS and CVD have the same range of MBP reactive T-cells in the CSF. This leads the researchers to posit that this immune reaction is secondary to damage in the CNS. Which makes me wonder....is the CSF of stroke patients and those with hypoxia or ischemic events regularly tested? And if so, are these people told they have an immune system disease? Obviously, the answer is no.


Myelin antigen reactive T cells in cerebrovascular diseases
W.Z.WANG,T.OLSSON,V.KOSTULAS,B.HOJEBERG,H.P.EKRE&H.LINK
Department of Neurology, Karolinska Institutet, Huddinge Hospital, Stockholm, Sweden

Quote:
INTRODUCTION In acute ischaemic cerebrovascular diseases (CVD), mononuclear cells appear in the brain parenchyma within 1-2 days and increase in number over the ensuing 5-30 days[1].Also in cerebrospinal fluid (CSF), elevated numbers of mononuclear cells may be detected. These cells are considered to mainly represent monocytes-macrophages, but there are no detailed studies on their lineage with,e.g.,antibodies to different cell surface markers. Oligoclonal IgG bands are present in the CSF while missing in corresponding serum, in about 10% of patients with CVD [2,3].A local B cell response directed to neurotropic viruses,as in patients with multiple sclerosis, has been reported in those patients with CVD who displayed oligoclonal IgG bands in CSF [4].Taken together,these observations indicate that patients with acute CVD may display an intrathecal immune response......

The strong increases in numbers of MBP, MBP peptide and PLP reactive T cells in blood, and of MBP reactive T cells in CSF, which we here report in our patients with Cerebro Vascular Disease, are in the same range as we have previously observed in MS [10,11].Thus, both diseases are accompanied by an expanded pool of myelin autoreactive T cells and they may well be secondary to damage to the central nervous system.

Here is the full paper in PDF form.
http://www.ncbi.nlm.nih.gov/pmc/article ... 8-0161.pdf

Frodo---but these t-cell mediated demylinating lesions are present in cerebrovascular disease, dementia, ischemic disease, carbon monoxide poisoning, etc. The t-cells react the exact same way.

right, Cece.
there are many demyelinating diseases, all have demyelination as a reaction to some insult of the CNS...ischemic, viral, bacterial, toxic, metabolic disorder, etc.

There's no need to place other demyelinating diseases under an "MS umbrella", Frodo. These other diseases can be explained and categorized by the known injury. Demyelination is secondary. The pathology is consistent....it's called demyelination.

There is only one demyelinating disease of unknown aetiology, it is called MS.

cheer

Distinction of demyelination [in MS] from destructive processes such as infarction depends largely on the demonstration of axons within regions of white matter that are devoid of myelin. This distinction is more obvious when grey matter is affected: in multiple sclerosis neurones are preserved (fig 1F​1F),), but this is not the case for infarction or other destructive processes that cause loss of myelin

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1860500/

I found this interesting...



... because neurons are not really preserved in MS.