Application of magnetization transfer imaging for intracranial lesions of tuberous sclerosis.

PURPOSE

Our goal was to assess the effectiveness of magnetization transfer imaging (MTI) and the usefulness of the magnetization transfer ratio (MTR) in tuberous sclerosis (TS).

METHOD

T2- and T1-weighted SE images with saturation pulse on/off before and after gadolinium enhancement in 10 patients with TS were obtained. The numbers of subependymal nodule (SEN), cortical tuber, and white matter (WM) abnormality detected on T1-, proton density, T2-, and MT T1-weighted SE images were compared. The contrast-to-noise ratio (C/N) on T1-, MT T1-, Gd T1-, and Gd MT T1-weighted SE images and MTR (1-Msat/MO) on each set of saturation/nonsaturation images for each lesions were calculated. Mean MTRs (mMTRs) of WM and gray matter (GM) from seven normal volunteers were also obtained.

RESULTS

MT T1-weighted SE images always depicted all lesions seen on conventional MRI and allowed depiction of more SENs (n = 80), cortical tubers (n = 197), and WM abnormalities (n = 82) than did T1-weighted (n = 58/85/33), proton density (n = 41/108/36), or T2-weighted (n = 48/121/46) SE images. The best C/N was obtained from Gd MT T1-weighted SE images in SENs and from MT T1-weighted SE images in other lesions. mMTRs of normal WM and GM were 36.43 and 29.42%, respectively. Cortical tubers and WM abnormalities had measured MTRs that were statistically equal to MTRs of GM in normal subjects (p < 0.005). MTRs of SENs showed lower mean (25.55%) and greater diversity (SD +/- 5.30), compared with MTRs of other lesions and normal GM and WM. One SEN with MTR of 20.72% was pathologically confirmed to be subependymal giant cell astrocytoma (SGCA). Nine SENs had measured MTR below 20.72% and six nodules among these were located in the region of the foramen of Monro, which is the characteristic location of SGCA.

CONCLUSION

MTI may be effective in detecting all cranial lesions of TS. MTR may increase the specificity of MRI because it can differentiate the histopathologic subtypes and track and evolution of SEN into SGCA.