Spinal cord samples (cervical, thoracic, lumbar) from 46 MS and 20 controls were stained for haematoxylin/eosin, elastin Van-Giessen, and Luxol Fast-Blue. Systematic assessment of measures of small vessel disease included vascular thickness, perivascular space dilation, fibrosis, hyalinotic changes, and myelin pallor. Fibrinogen, a marker for blood-brain barrier integrity, was examined in a subset of 42 MS and 6 controls using quantitative and semiquantitative methods.
Controls showed age-related vascular thickening with hyalinotic and fibrotic changes, and perivascular space dilation. In non-lesional tissue, MS cases had 89% more vascular fibrosis (p=0.002) than controls. In non-lesional white matter, myelin pallor increased by 66% (p<0.001) in MS compared to controls with both groups showing a symmetrical topographical pattern of myelin pallor. Perivascular space dilation increased by 93% in white (p<0.001) and 82% in grey matter (p<0.001) compared to controls. Striking fibrinogen deposition was observed in non-lesional MS areas, both extracellularly and within hypertrophic astrocytes. Extracellular fibrinogen was over 200 times more common in MS (p<0.0001) and correlated with increased inflammation and faster rate to wheelchair dependency. Fibrinogen-positive astrocyte coverage increased by 247% and hypertrophy by 83% (both p<0.001), both correlating with age at wheelchair dependence. MS lesions showed a further increase in vascular fibrosis, extracellular and astrocytic fibrinogen compared to the surrounding non-lesional tissue (all p<0.001).
These findings highlight that vascular abnormalities and blood-brain barrier leakage outside the paradigmatic demyelinated lesion are key features of MS spinal cord pathology and relate to inflammation and disease severity.