Objective: To determine the pathologic basis of areas not exhibiting signal
of the short-T2 component of the T2 relaxation distribution in MS, as stud
ied in formalin-fixed brain. Background: A myelin-specific MRI signal would
be of great importance in assessing demyelination in patients with MS. Evi
dence indicates that the short-T2 (10 to 50 millisecond) component of the T
2 relaxation distribution originates from water in myelin sheaths. The auth
ors present two cases of MS in which the anatomic distribution of the short
-T2 component was correlated with the pathologic findings in postmortem for
malin-fixed brain. Method: One half of the formalin-fixed brain was suspend
ed in a gelatin-albumin mixture cross-linked with glutaraldehyde, and scann
ed with a 32-echo MRI sequence. The brain was then cut along the center of
the 5-mm slices scanned, photographed, dehydrated, and embedded in paraffin
. Paraffin sections, stained with Luxol fast blue and immunocytochemically
for 2',3'-cyclic nucleotide 3'-phosphohydrolase for myelin and by the Biels
chowsky technique for axone, were compared with the distribution of the amp
litude of the short-T2 component of the comparable image slices. Results: T
he anatomic distribution of the short-T2 component signal corresponded to t
he myelin distribution. Chronic, silent MS plaques with myelin loss correla
ted with areas of absence of short-T2 signal. The numbers of axone within l
esions were reduced, but many surviving axons were also seen in these areas
of complete loss of myelin. Conclusion: In formalin-fixed MS brains the sh
ort-Ta component of the T2 relaxation distribution corresponds to the anato
mic distribution of myelin. Chronic, silent demyelinated MS plaques show ab
sence of the short-Ta component signal. These results support the hypothesi
s that the short-T2 component originates from water related to myelin.