Grey Matter

G

I read this paper and it says Grey Matter is the thing to monitor and then we go at a trial and its whole brain atrophy. Why?

Association of Gray Matter Atrophy Patterns with Clinical Phenotype and Progression in Multiple Sclerosis.Rocca MA, Valsasina P, Meani A, Gobbi C, Zecca C, Rovira A, Sastre-Garriga J, Kearney H, Ciccarelli O, Matthews L, Palace J, Gallo A, Bisecco A, Lukas C, Bellenberg B, Barkhof F, Vrenken H, Preziosa P, Filippi M; MAGNIMS Study Group.Neurology. 2021 Jan 13:10.1212/WNL.0000000000011494

Objectives: Grey matter (GM) involvement is clinically relevant in multiple sclerosis (MS). Using source-based morphometry (SBM), we characterized GM atrophy and its 1-year evolution across different MS phenotypes.

Methods: Clinical and MRI data were obtained at 8 European sites from 170 healthy controls (HCs) and 398 MS patients (34 clinically isolated syndromes [CIS], 226 relapsing-remitting [RR], 95 secondary progressive [SP] and 43 primary progressive [PP] MS). Fifty-seven HC and 144 MS underwent 1-year follow-up. Baseline GM loss, atrophy progression and correlations with disability and 1-year clinical worsening were assessed.

Results: SBM identified 26 cerebellar, subcortical, sensory, motor and cognitive GM components. GM atrophy was found in MS vs HC in almost all components (p=range<0.001-0.04). Compared to HCs, CIS patients showed circumscribed subcortical, cerebellar, temporal and salience GM atrophy, while RRMS patients exhibited widespread GM atrophy. Cerebellar, subcortical, sensorimotor, salience and fronto-parietal GM atrophy was found in PPMS patients vs HCs, and SPMS vs RRMS. At 1-year, 21 (15%) patients had clinically worsened. GM atrophy progressed in MS in subcortical, cerebellar, sensorimotor, and fronto-temporo-parietal components. Baseline higher disability was associated (R2=0.65) with baseline lower normalized brain volume (beta=-0.13, p=0.001), greater sensorimotor GM atrophy (beta=-0.12, p=0.002) and longer disease duration (beta=0.09, p=0.04). Baseline normalized GM volume (odds ratio=0.98, p=0.008) and cerebellar GM atrophy (odds ratio=0.40, p=0.01) independently predicted clinical worsening (area-under-the-curve=0.83).

Conclusion: GM atrophy differed across disease phenotypes and progressed at 1-year in MS. In addition to global atrophy measures, sensorimotor and cerebellar GM atrophy explained baseline disability and clinical worsening.

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  • As computer algorithms take over ‘brain mapping’ of all sorts (voxel based or source-based), the average radiologist (and hopefully NEURO-radiologist) knows some of these mathematical modeling terminology since everything is changing since MOST neurologists are at sea once 3D imaging modalities are brought into play. Add to this the US FDA approval of 7T MRI imagery that I myself have not seen (have been in the field of MS for 2 decades and in medicine for 4 decades) and most of us in the Universities across the USA (let alone the world) do NOT have 7T MRIs, we have no idea what the images look like, except to read a stray article here and there. So, you get the point. Math, modeling and 3D imagery is all smoke and mirrors for the average radiologist, let alone a neurologist. And sophisticated ultra-high strength MRIs were approved in 2017 and remain enveloped in mystery for MOST of us. How then can we comprehend the nuances of VBM or SBM intricacies ?

    That the cortex is involved in CIS is a well known fact, probably about 2 decades ago (?). While regional, posterior fossa structures, deep gray matter structure involvement, etc keep coming up in ‘analyses’ with one more paper being churned out is NOT surprising. What is surprising to me is that the FDA has ALSO approved volumetric analyses (NeuroQuant and Icometrix) done by these two companies for MR of brain images for MS, for instance, and YET not one University that I know of (in a general sense) uses these. I tried to get any one of them to set up shop at my Univ with zero success.

    Moral: We read papers, write papers, publish, etc, but practice ? That’s another story. Most medical Univs do not have a good imaging/computer lab that one can work with. So we cannot and do not use FDA approved products on the one hand and certainly do not have computer geeks running around in major Universities so we end up doing mostly, nothing. A familiar tale ?

  • What’s the relationship between demyelination and brain atrophy in MS? There’s a lot of talk about neuroplasticity, could the brain atrophy cause the compounding disabilities rather than demyelination?

  • What methods were used to measure GM atrophy, progression, and correlation to disabilitY ? The abstract doesn’t indicate. Are any of these measurement tools, methods, types of clinical observations, avail to neuros now to help inform dmd management of pwm?

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