Abstract
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Highlights
Neocortical grey matter demyelination, microglial activation and neurodegeneration, which may in-part be driven by inflammation of the overlying leptomeninges, are important pathological processes influencing the clinical severity and outcome of multiple sclerosis (MS)[1]
White matter lesion area was unchanged when compared with the progressive MS cases with little subpial cortical demyelination
Analysis of whole coronal macrosections reveals cortical demyelination is more extensive than reported by conventional histological methods
Summary
Neocortical grey matter demyelination, microglial activation and neurodegeneration, which may in-part be driven by inflammation of the overlying leptomeninges, are important pathological processes influencing the clinical severity and outcome of multiple sclerosis (MS)[1]. Neocortical and cerebellar cortical pathology is evident from the earliest stages of MS[2,3,4,5]. It is a pathological hallmark of progressive MS[1,2] and closely associates with clinical severity at all stages[6]. The extent of cortical pathology is better at predicting disease outcome than white matter pathology[7]. Radiological imaging of grey matter and cortical atrophy are predictive of the conversion to clinically definite MS[8,9,10] or the risk of transitioning to the progressive phase and disability[7,11]. Even high fidelity, non-routine, imaging technologies fail to identify lesions of the most superficial cortical layers, whilst neuropathological assessment of standard size tissue blocks often underestimates the extent of cortical lesions, which can occupy the cortical ribbon over multiple contiguous gyri and sulci[2,12]
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