“I was asked by a colleague in Porto last week whether or not I let the presence or absence of brain atrophy on MRI affect my clinical decision making about DMTs and treatment? I had to think about the question and haven’t stopped thinking about it since. The first problem is that our neuroradiologists don’t routinely report brain atrophy, unless it is gross atrophy, i.e. easy to see with the naked eye. Although we know that brain atrophy occurs early in the disease course it is often very subtle and difficult to assess with the naked eye; it has to be assessed using post-acquisition data processing tools. In other words the neuroradiologist has to arrange for the images to be analysed off-line for atrophy and to then compare the results with a previous scans or to a normative data set. At the moment brain atrophy measurements are not a routine in our hospital, although we do collect the correct MRI sequences to measure atrophy.”
Scenario 1 – in a recently diagnosed person with MS with active MS has a low or moderate lesion load, would the presence of brain atrophy at baseline push you towards a more aggressive therapy, i.e. a drug that affects brain atrophy, or would you be comfortable with that person choosing interferon-beta or glatiramer acetate?
Fisher E, Lee JC, Nakamura K, Rudick RA. Gray matter atrophy in multiple sclerosis: a longitudinal study. Ann Neurol. 2008 Sep;64(3):255-65. doi: 10.1002/ana.21436.
OBJECTIVE: To determine gray matter (GM) atrophy rates in MSers at all stages of disease, and to identify predictors and clinical correlates of GM atrophy.
METHODS: MSers and healthy control subjects were observed over 4 years with standardized magnetic resonance imaging (MRI) and neurological examinations. Whole-brain, GM, and white matter atrophy rates were calculated. Subjects were categorized by disease status and disability progression to determine the clinical significance of atrophy. MRI predictors of atrophy were determined through multiple regression.
RESULTS: Subjects included 17 healthy control subjects, 7 subjects with clinically isolated syndromes, 36 MSers with relapsing-remitting MS (RRMS), and 27 MSers with secondary progressive MS (SPMS). Expressed as fold increase from control subjects, GM atrophy rate increased with disease stage, from 3.4-fold normal in CISers converting to RRMS to 14-fold normal in SPMS. In contrast, white matter atrophy rates were constant across all MS disease stages at approximately 3-fold normal. GM atrophy correlated with disability. MRI measures of focal and diffuse tissue damage accounted for 62% of the variance in GM atrophy in RRMS, but there were no significant predictors of GM atrophy in SPMS.
INTERPRETATION: Gray matter tissue damage dominates the pathological process as MS progresses, and underlies neurological disabillity. Imaging correlates of gray matter atrophy indicate that mechanisms differ in RRMS and SPMS. These findings demonstrate the clinical relevance of gray matter atrophy in MS, and underscore the need to understand its causes.
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