Saturday, 14 September 2013

Ventricles Enlarge as the Brain shrinks

Simon JH, Jacobs LD, Campion MK, Rudick RA, Cookfair DL, Herndon RM, Richert JR, Salazar AM, Fischer JS, Goodkin DE, Simonian N, Lajaunie M, Miller DE, Wende K, Martens-Davidson A, Kinkel RP, Munschauer FE 3rd, Brownscheidle CM.A longitudinal study of brain atrophy in relapsing multiple sclerosis. The Multiple Sclerosis Collaborative Research Group (MSCRG).Neurology. 1999;53:139-48.

OBJECTIVE:To determine if progressive brain atrophy could be detected over 1- and 2-year intervals in relapsing MS, based on annual MR studies from the Multiple Sclerosis Collaborative Research Group (MSCRG) trial of interferon beta-1a (Avonex).
METHODS:All subjects had mild to moderate disability, with baseline expanded disability status scores ranging from 1.0 to 3.5, and at least two relapses in the 3 years before study entry. Atrophy measures included third and lateral ventricle width, brain width, and corpus callosum area.
RESULTS:Significant increases were detected in third ventricle width at year 2 and lateral ventricle width at 1 and 2 years. Significant decreases in corpus callosum area and brain width were also observed at 1 and 2 years. Multiple regression analyses suggested that the number of gadolinium-enhancing lesions at baseline was the single significant contributor to change in third ventricle width. Atrophy over 1 and 2 years as indicated by enlargement of the third and lateral ventricle and shrinkage of the corpus callosum was greater for patients entering the trial with enhancing lesions. Greater disability increments over 1 and 2 years were associated with more severe third ventricle enlargement.
CONCLUSION: In patients with relapsing MS and only mild to moderate disability, significant cerebral atrophy is already developing that can be measured over periods of only 1 to 2 years. The course of cerebral atrophy in MS appears to be influenced by prior inflammatory disease activity as indicated by the presence of enhancing lesions. Brain atrophy measures are important markers of MS disease progression because they likely reflect destructive and irreversible pathologic processes.
You can see lateral ventricle getting bigger and more crenulated as the brain shrinks. 
The above is a brain from Huntingtons disease. 

You said is it just the third ventricle that enlarges as the brain shrinks, well as can be seen from this post it occurs in other ventricles and can be seen in the picture below as the lateral ventricles (left and right) are enlarging

7 comments:

  1. If it is possible to stop or delay the brain atrophy with some kind of neuroprotective DMT.

    Is it then likely that such neuroprotective drugs will work the same in Alzheimer's and e.g. Huntington's ( the picture included in the post above ). Or is it more likely that the "brain atrophy" part of the disease differs between MS and other dementias?

    I'm just wonder if this "neuroprotection dmt's" can have a much wider benefit for patients with other dementias.

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    1. We believe that there is a good chance of drugs that are neuroprotective in one disease may be useful in another disease, but the proof is in the pudding. At the moment there are no wonder drugs for neuroprotection and there are differences between MS and other diseases but it may be parts of a spectrum and MS is on one pole and others are on a different pole because there commonalities between MS and other conditions

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  2. However look at posts a few days ago and fluoxitine the ACE inhibitor bit the dust. However I think drugs have better chance of success in MS as the damage accumulates more slowly.

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  3. Thank you for swift reply!

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  4. "The course of cerebral atrophy in MS appears to be influenced by prior inflammatory disease activity as indicated by the presence of enhancing lesions."

    If this were the case, would you expect the rate of atrophy to slow for any MSer who had NEDA for a few years on their DMT? Has that been measured?

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  5. If people take DMT, say tysabri, it has been shown that markers of atrophy drop

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  6. I take Tysabri on the basis of Italian studies that show a reduction in brain atrophy. While lesions can heal, it looks like atrophy would be permanent, esp. because neurons don't regrow, and while long considered a "white matter" disease (I know the brain is from a different disease process) it looks like in the pic the gray matter is primarily affected. My neuro says that not everyone experiences atrophy, but it doesn't look like the odds are in my favor. What is driving this atrophy? Are immune cells picking off myelin and reducing volume, but the neurons are or could be still intact?

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