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Updated: Aug 2, 2026
Diffusion Tensor Magnetic Resonance Imaging in the Analysis of Neurodegenerative Diseases
Published on: July 28, 2013
A pathology-MRI study of the short-T2 component in formalin-fixed multiple sclerosis brain
G R Moore1, E Leung, A L MacKay
1Department of Pathology and Laboratory Medicine, Vancouver General Hospital, Vancouver, BC, Canada. wmoore@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
Insights
The short-T2 MRI signal in multiple sclerosis (MS) brains directly reflects myelin distribution. Absence of this signal accurately identifies chronic, silent MS plaques with significant myelin loss.
Area of Science:
- Neuroimaging
- Pathology
- Multiple Sclerosis (MS) Research
Background:
- A myelin-specific MRI signal is crucial for assessing demyelination in MS.
- The short-T2 component (10-50 ms) of T2 relaxation distribution is linked to water within myelin sheaths.
- This study correlates short-T2 signal distribution with pathologic findings in postmortem MS brains.
Purpose of the Study:
- To investigate the pathological basis of areas lacking the short-T2 MRI signal in MS.
- To validate the origin of the short-T2 component as myelin-related water.
Main Methods:
- Formalin-fixed human brains from MS patients were scanned using a 32-echo MRI sequence.
- Brains were sectioned, processed, and stained for myelin (Luxol fast blue, 2',3'-cyclic nucleotide 3'-phosphohydrolase) and axons (Bielschowsky technique).
- The distribution of the short-T2 signal amplitude was compared with myelin and axon pathology.
Main Results:
- The short-T2 MRI signal distribution precisely matched the anatomic distribution of myelin.
- Areas with chronic, silent MS plaques and myelin loss showed a complete absence of the short-T2 signal.
- While axon numbers were reduced in these plaques, surviving axons were present despite complete myelin loss.
Conclusions:
- The short-T2 component of T2 relaxation in formalin-fixed MS brains accurately represents myelin distribution.
- Absence of the short-T2 signal signifies chronic, silent demyelinated MS plaques.
- These findings support the hypothesis that the short-T2 component originates from myelin-associated water.
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These technologies include computerized axial tomography (CAT or CT scans), positron-emission tomography (PET scans), magnetic resonance imaging (MRI), functional magnetic resonance imaging (fMRI), and Transcranial Magnetic Stimulation (TMS).