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Effect of T1 Relaxation Time on Lesion Contrast Enhancement in FLAIR MR Imaging

A Study Using Computer-Generated Brain Maps

Elias R. Melhem1 and Ryuta Itoh1

1 Both authors: Department of Radiology and Radiological Sciences, The Johns Hopkins Hospital, The Johns Hopkins Medical Institutions, 600 N. Wolfe St., Baltimore, MD 21287-2182.



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  		Fig. 1. —Computer-generated T2-weighted (left image) and fluid-attenuated inversion recovery (FLAIR) maps (center image, 40 msec; right image 140 msec) show 12 simulated lesions placed in white matter of cerebral hemisphere parallel to lateral ventricle. T1 relaxation time of lesions varied from 800 msec (posteriormost lesion) to 3000 msec (anteriormost lesion) by increments of 200 msec. All simulated lesions were hyperintense to white matter on T2-weighted maps. On FLAIR maps, simulated lesions changed from hyperintense to hypointense with increasing T1 relaxation time. Lesions with identical T1 relaxation times were hypointense on short-TE FLAIR and hyperintense on long-TE FLAIR (arrowheads). Also, lesions that were hyperintense on T2-weighted sequences were invisible on FLAIR sequences (circles).

 


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  		Fig. 2. —Graph shows isointense T1 (T1 relaxation time at which simulated lesion with T2 relaxation time of 300 msec became isointense to surrounding white matter) versus TE on corresponding fluid-attenuated inversion recovery map. White area = hypointense, gray area = hyperintense.

 


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  		Fig. 3. —8-year-old boy with cerebral adrenoleukodystrophy. Axial T1-weighted MR image (TR/TE, 516/14) (left image) at level of lateral ventricles shows low signal intensity (prolonged T1 relaxation time) involving splenium of corpus callosum and deep white matter of both frontal and parietooccipital lobes. Axial T2-weighted MR image (3000/100) (center image) shows corresponding high signal intensity (prolonged T2 relaxation time) in involved regions. Axial fluid-attenuated inversion recovery MR image (TR/TI/TE, 6000/2000/53) (right image) shows low signal intensity in center (asterisks) and high signal intensity in periphery (arrowheads) of white matter lesion in both parietooccipital lobes. The low signal intensity in center of lesion is presumably a result of more severely damaged white matter and greater prolongation of T1 relaxation time.

 

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