http://www.ncbi.nlm.nih.gov/pubmed/22499842Subcortical and Cortical Gray Matter Atrophy in a Large Sample of Patients with Clinically Isolated Syndrome and Early Relapsing-Remitting Multiple Sclerosis.
Significant SDGM, but not cortical, atrophy develops during the first 4 years of the RRMS. GM atrophy is relevant for disease progression from the earliest clinical stages.
http://www.ajnr.org/content/early/2012/03/29/ajnr.A3030Patients with CIS showed significantly increased content and volume of iron, as determined by abnormal SWI-phase measurement, in the various SDGM structures, suggesting that iron deposition may precede structure-specific atrophy.
http://www.ncbi.nlm.nih.gov/pubmed/23296131A number of clinical observations as well as recent neuropathologic and neuroimaging studies have clearly demonstrated extensive involvement of the thalamus, basal ganglia, and neocortex in patients with MS. Modern MRI techniques permit visualization of GM lesions and measurement of atrophy. These contemporary methods have fundamentally altered our understanding of the pathophysiologic nature of MS. Evidence confirms the contention that GM injury can be detected in the earliest phases of MS, and that iron deposition and atrophy of deep gray nuclei are closely related to the magnitude of inflammation. Extensive involvement of GM, and particularly of the thalamus, is associated with a wide range of clinical manifestations including cognitive decline, motor deficits, fatigue, painful syndromes, and ocular motility disturbances in patients with MS. In this review, we characterize the neuropathologic, neuroimaging, and clinical features of thalamic involvement in MS. Further, we underscore the contention that neuropathologic and neuroimaging correlative investigations of thalamic derangements in MS may elucidate not heretofore considered pathobiological underpinnings germane to understanding the ontogeny, magnitude, and progression of the disease process.
I don't know about that this time, Harry....this recent paper includes some MS name researchers, including Dr. Eliot Frohman and Dr. Barnett. The evidence about the importance of gray matter atrophy is compiling. What will be interesting is how this will be explained--does the iron deposition come first, or is it initiated by the inflammatory process? Drug companies will go for the inflammatory observations, and start looking at cessation of gray matter atrophy as a marker of their products' efficacy.HarryZ wrote:Hi Cheer,
I can imagine the established world of MS medicine is already working on a way to try and discredit these findings. They've done in the past and they will do it the future. A lot of money is at issue here and any research that threatens this will be quickly attacked.
Harry
Hi Cheer,I don't know about that this time, Harry....this recent paper includes some MS name researchers, including Dr. Eliot Frohman and Dr. Barnett.
While I can understand a doc's hesitation to endorse a procedure that is very new and does not yet have a lot of scientific backing to it, it's the "dismissal" or "bad-mouthing" attitude that gets launched immediately! Unfortunately new discoveries like CCSVI threaten the established theories on MS and a lot of money and personal reputations can hang in the balance. It would be nice if the "established" group would just say the new theory is interesting so let those who talk about provide the science to try and prove it.CureOrBust wrote:I use two different Neurologists, at two different locations. One of them is Prof John Pollard, who is very well respected within the "establishment" of MS treatment, worldwide; I think he also won an an award from the Australian Govt a few years back. When I first brought CCSVI to his attention, he quickly dismissed it because of its lack of backing within the (his) accepted group of respected neurologists.
What gives me GREAT hope here, is that Barnet shares an office with Prof Pollard and has shared credit on published papers, and now Barnet is obviously speaking with Zivadinov. I would be surprised if Barnet and Pollard do not speak about things like this "around the water cooler". Its not in your face CCSVI, but I think its small "leakage" like this that has a great potential to bring CCSVI research into the realm of the "respected" neurologists.
Exactly, Cure! Barnett discussing the reasons for gray matter atrophy with Zivadinov is encouraging. The fact that Eliot Frohman, who was at the first CCSVI conference and collaborated on this gray matter study, is another interesting development. BNAC has been publishing some important research on the changes that happen after venoplasty---one presented at ECTRIMS showed increased cerebral spinal fluid flow in all pwMS treated with venoplasty. http://registration.akm.ch/einsicht.php ... KEN_ID=900CureOrBust wrote:I use two different Neurologists, at two different locations. One of them is Prof John Pollard, who is very well respected within the "establishment" of MS treatment, worldwide; I think he also won an an award from the Australian Govt a few years back. When I first brought CCSVI to his attention, he quickly dismissed it because of its lack of backing within the (his) accepted group of respected neurologists.
What gives me GREAT hope here, is that Barnet shares an office with Prof Pollard and has shared credit on published papers, and now Barnet is obviously speaking with Zivadinov. I would be surprised if Barnet and Pollard do not speak about things like this "around the water cooler". Its not in your face CCSVI, but I think its small "leakage" like this that has a great potential to bring CCSVI research into the realm of the "respected" neurologists.
Hi mmpetunia--mmpetunia wrote:Cheerleader,
you mentioned that you are keeping a close eye on the grey matter atrophy on your husbands MRI scans. i was under the impression that grey matter is not easily visible on MRI. how are you able to look at the grey matter? i would definitely be interested in keeping tabs on mine. also, the OCT eye scan, where/how are you getting this done? is this paid for out of pocket or can i request via my neuro?
The five-year study, which covered 180 patients, also found that thalamic atrophy has p0tential as a way to evaluate novel therapies for MS, according to Eva Havrdova, MD, PhD, principal investigator.
“The thalamus is providing us with a new window on MS,” says Robert Zivadinov, MD, PhD, UB professor of neurology, BNAC director and leader of the research team. “In our recent studies, we have used large datasets to investigate the evolution of atrophy of the thalamus and its association with clinical impairment in MS, starting with the earliest stages of the disease. The location of the thalamus in the brain, its unique function and its vulnerability to changes wrought by the disease make the thalamus a critical barometer of the damage that MS causes to the brain.”
“Since progressive pathology of the thalamus has been shown in all different MS disease types, including in pediatric MS patients, we must look at the thalamus as a biomarker for assessing new therapies,” says Zivadinov. “Measurement of thalamic atrophy may become an ideal MRI outcome for MS clinical trials.
“Atrophy in MS patients happens in the thalamus more rapidly than in other brain structures,” Zivadinov continues. “It is detectable very early in the disease and it is less affected by fluid shifts in the brain, an effect of anti-inflammatory drugs used in MS. This feature in particular, makes thalamic atrophy an ideal candidate for assessing novel therapies.”
Hi Daniel--daniel wrote:Thanks for the update cheer! Does this also mean pathology of the thalamus is related to bloodflow/hypoxia?
Cheer,Dr. Zivadinov (a real neurologist) is asking if it's time to look at MS as a disease of the gray matter.
This is a radical shift, since, as Harry notes---the drugs on the market were not created to address gray matter degradation. It's as if Dr. Zivadinov is saying, we're back to square one...the days before EAE. That's pretty interesting.
cheer
