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Isolating Central Nervous System Tissues and Associated Meninges for the Downstream Analysis of Immune cells
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Meningeal inflammation is not associated with cortical demyelination in chronic multiple sclerosis

Evert-Jan Kooi1, Jeroen J G Geurts, Jack van Horssen

  • 1Departments of Pathology (Neuropathology) University Medical Center, Amsterdam, The Netherlands. e.kooi@vumc.nl

Journal of Neuropathology and Experimental Neurology
|August 15, 2009
PubMed

Insights

Cortical demyelination in chronic multiple sclerosis (MS) is extensive. However, meningeal inflammation does not correlate with these cortical lesions, suggesting alternative disease mechanisms in MS.

Area of Science:

  • Neuroimmunology
  • Neuropathology

Background:

  • Cortical demyelination is a significant feature in chronic multiple sclerosis (MS).
  • The pathogenesis of cortical lesions in MS remains unclear, as they lack typical inflammatory markers.

Purpose of the Study:

  • To investigate the relationship between leptomeningeal inflammation and cortical demyelination in chronic MS.
  • To analyze the cellular composition of meningeal infiltrates in relation to cortical lesions.

Main Methods:

  • Autopsy brain samples from 28 chronic MS patients and 6 controls were analyzed.
  • Immunohistochemistry was used to identify various immune cells in meningeal tissues.
  • Morphometric analysis assessed subpial demyelination and its correlation with meningeal inflammation.

Main Results:

  • Significant meningeal inflammation, predominantly T cells, was observed in chronic MS patients.
  • No correlation was found between the extent of subpial demyelination and meningeal inflammation.
  • Meningeal infiltrates did not differ in areas adjacent to cortical lesions versus normal-appearing gray matter.

Conclusions:

  • Meningeal inflammation is not directly associated with cortical demyelination in a majority of chronic MS patients.
  • The findings suggest that other mechanisms may drive cortical lesion formation in MS.
  • Absence of follicle-like structures further challenges common inflammatory models for cortical MS lesions.

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