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From the Departments of Pathology and Laboratory Medicine (Dr. Moore and Ms. Leung), Radiology (Drs. MacKay, Vavasour, Whittall, and Li), Physics (Dr. MacKay and Mr. Cover), and Medicine (Neurology) (Drs. Hashimoto, Oger, and Paty), University of British Columbia; the Departments of Pathology and Laboratory Medicine (Dr. Moore), Radiology (Dr. Li), and Medicine (Neurology) (Drs. Hashimoto, Oger, and Paty), Vancouver Hospital and Health Sciences Centre, Vancouver, British Columbia, Canada; and Research Services (Dr. Sprinkle), Veterans Affairs Medical Center, Augusta, GA.
Address correspondence and reprint requests to Dr. G.R.W. Moore, Department of Pathology and Laboratory Medicine, Vancouver General Hospital, Room 1302, 910 West 10th Avenue, Vancouver BC, Canada V5Z 1L8; e-mail: wmoore{at}vanhosp.bc.ca
OBJECTIVE: To determine the pathologic basis of areas not exhibiting signal of the short-T2 component of the T2 relaxation distribution in MS, as studied in formalin-fixed brain.
BACKGROUND: A myelin-specific MRI signal would be of great importance in assessing demyelination in patients with MS. Evidence indicates that the short-T2 (10 to 50 millisecond) component of the T2 relaxation distribution originates from water in myelin sheaths. The authors present two cases of MS in which the anatomic distribution of the short-T2 component was correlated with the pathologic findings in postmortem formalin-fixed brain. Method: One half of the formalin-fixed brain was suspended in a gelatin-albumin mixture cross-linked with glutaraldehyde, and scanned 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 Bielschowsky technique for axons, were compared with the distribution of the amplitude of the short-T2 component of the comparable image slices.
RESULTS: The anatomic distribution of the short-T2 component signal corresponded to the myelin distribution. Chronic, silent MS plaques with myelin loss correlated with areas of absence of short-T2 signal. The numbers of axons within lesions were reduced, but many surviving axons were also seen in these areas of complete loss of myelin.
CONCLUSION: In formalin-fixed MS brains the short-T2 component of the T2 relaxation distribution corresponds to the anatomic distribution of myelin. Chronic, silent demyelinated MS plaques show absence of the short-T2 component signal. These results support the hypothesis that the short-T2 component originates from water related to myelin.1510
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