Neurology: Multiple sclerosis: different clinical types, the corresponding gray matter involvement types are different

In the past few decades, gray matter (GM) involvement has increasingly been recognized as an important component of the pathophysiology of multiple sclerosis (MS).
GM atrophy occurs in the earliest stage of MS and progresses over time.
The atrophy rate of patients with relapsing-remitting MS (RRMS) is twice that of the control group, while the atrophy rate of patients with progressive MS is as high as twice.

There has always been a substantial relationship between GM atrophy and clinical disability.
The areas of GM atrophy are not evenly distributed among the phenotypes.
Deep GM and parietal lobes are affected earlier.
In the later stages of the disease, GM loss gradually spreads to the frontal, temporal, occipital, and cerebellar regions.

Maria A.
Rocca and others at Vita-Salute San Raffaele University in Italy used source-based morphometry (SBM) to explore the characteristics of GM atrophy and the 1-year evolution of this atrophy in different MS phenotypes.

They enrolled 170 healthy controls (HCs) and 398 MS patients (34 clinically isolated syndrome [CIS], 226 relapsing-remitting MS [RRMS], and 95 secondary progressive MS from 8 European stations.
[SPMS], clinical and MRI data were obtained from 43 primary progressive MS [PPMS]).
Fifty-seven HC and 144 MS patients were followed up for 1 year.
The baseline GM loss, the progression of atrophy, and the correlation with disability and 1-year clinical deterioration were also evaluated.

They identified 26 cerebellar, subcortical, sensory, motor, and cognitive GM components through SBM.

Compared with HC, in MS, GM atrophy is found in almost all components; CIS patients show circular subcortical, cerebellar, temporal and significant GM atrophy, while RRMS patients show extensive GM atrophy.

The GM atrophy of the cerebellum, subcortex, sensorimotor, and frontal parietal lobe in PPMS patients, and GM atrophy in SPMS and RRMS patients.

At 1 year, 21 patients (15%) had worsened clinical conditions.
GM atrophy in MS progresses in subcortical, cerebellar, sensorimotor, and anterior temporal parietal components.
Disability at a higher baseline vs.
normalized brain volume at a lower baseline (β = -0.
13, p = 0.
001), greater sensorimotor GM atrophy (β = -0.
12, p = 0.
002), and a longer course (β = 0.
09, p = 0.
04) Correlation (R2 = 0.
65).

Baseline normalized GM volume (OR 0.
98, p = 0.
008) and cerebellar GM atrophy (OR 0.
40, p = 0.
01) independently predicted clinical deterioration (area under the curve 0.
83).

The important significance of this study lies in the discovery: GM atrophy is different in different disease phenotypes, and it continues to progress in the year after MS.
In addition to global atrophy measures, sensorimotor and cerebellar GM atrophy can explain baseline disability and clinical deterioration.

Original Source:
neurology.
org/content/96/11/e1561" target="_blank" rel="noopener">Association of Gray Matter Atrophy Patterns With Clinical Phenotype and Progression in Multiple Sclerosis