Wednesday, 21 December 2016

Sodium now its cognitive impairment

Maarouf A, Audoin B, Pariollaud F, Gherib S, Rico A, Soulier E, Confort-Gouny S, Guye M, Schad L, Pelletier J, Ranjeva JP, Zaaraoui W.Increased total sodium concentration in gray matter better explains cognition than atrophy in MS. Neurology. 2016 Dec 14. pii: 10.1212/WNL.0000000000003511. [Epub ahead of print]

OBJECTIVE:To investigate whether brain total sodium accumulation assessed by 23Na MRI is associated with cognitive deficit in relapsing-remitting multiple sclerosis (RRMS).
METHODS:Eighty-nine participants were enrolled in the study (58 patients with RRMS with a disease duration ≤10 years and 31 matched healthy controls). Patients were classified as cognitively impaired if they failed at least 2 tasks on the Brief Repeatable Battery. MRI was performed at 3T using 23Na MRI to obtain total sodium concentration (TSC) in the different brain compartments (lesions, normal-appearing white matter [NAWM], gray matter [GM]) and 1H- magnetization-prepared rapid gradient echo to assess GM atrophy (GM fraction).
RESULTS: The mean disease duration was 3.1 years and the median Expanded Disability Status Scale score was 1 (range 0-4.5). Thirty-seven patients were classified as cognitively preserved and 21 as cognitively impaired. TSC was increased in GM and NAWM in cognitively impaired patients compared to cognitively preserved patients and healthy controls. Voxel-wise analysis demonstrated that sodium accumulation was mainly located in the neocortex in cognitively impaired patients. Regression analysis evidenced than the 2 best independent predictors of cognitive impairment were GM TSC and age. Receiver operating characteristic analyses demonstrated that sensitivity and specificity of the GM TSC to classify patients according to their cognitive status were 76% and 71%, respectively.
CONCLUSIONS: This study provides 2 main findings. (1) In RRMS, total sodium accumulation in the GM is better associated with cognitive impairment than GM atrophy; and (2) total sodium accumulation in patients with cognitive impairment is mainly located in the neocortex.


We have shown that sodium channel blockers can be neuroprotective, so when imagers began to image sodium in the brain they said is was associated with neurodegeneration. But now in this study they say it is not really associated with neurodegeneration, but is now associated with cognitive impairment.

When we look at the figures it is not that clear cut and this is the central problem with imaging. This is a tool used to find something in a complex biology, which can not be proven in the living individual that they are using to define the outcome. 

This is yet another example occuring over an over with the clinical imagers. 

Defining the biology may help describe what they are seeing, presumably during demyelination the sodium channels redistribute allowing the machine to see something that is usually restricted to the Nodes of Ranvier, but here I go....spouting perhaps nonsense but surely it is just as plausible and i haven't been near an image.

However it should be said that essentially no imaging outcome provides anything that links to tangible pathology and the literature is full of wishy-washy correlations that mean nothing to the individual because the associations between the outcome and the imaging parameter is so, so weak. 

Recently I was asked to defend the  statement posed by an imager for a journal "We should not be funding animal studies of MS".

I questioned whether this was an appropriate way to debate the value of animal models, (it is a destructive line of argument and to me-smacks of arrogance) and said that I hope they likewise debate 

" Academic phase III clinical trials in MS go nowhere and should not be funded?" :-(

and

"We should not be funding imaging studies in MS"

It is a useful tool but let's face it, it has had its day:-) and this produces as much tosh as dogey animal studies. (Arrogant...Moi?)

I said that I would do it, but I would not try to defend everybodies animal studies. The world has moved-on as there are treatment options available for some and should we be using severe animal models to address fundemental questions that can be addressed using less severe systems.

I suggested they get some hard core animal immunologist to do it...then they will get what the questioner wants...a noose to wrap round the researchers neck.

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