| Co-Investigator(Kenkyū-buntansha) |
HIGANO Shuichi School of Medicine, Tohoku University Assistant professor, 医学部, 助手 (20173148)
KITAMOTO Tetsuyoki School of Medicine, Tohoku University Professor, 医学部, 教授 (20192560)
坂本 澄彦 東北大学, 医学部, 教授 (20014029)
岩崎 祐三 東北大学, 医学部, 教授 (00142927)
|
|---|
| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1996: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1995: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1994: ¥800,000 (Direct Cost: ¥800,000)
|
|---|
| Research Abstract |
We investigated sequential MR imaging findings of hypoxic encephalopathy and correlated them with histological findings at autopsy. We retrospectively reviewed sequential MR imaging studies of the brain in 6 patients with hypoxic brain damage. Sequential changes in signal intensity and morphological features of the brain were evaluated on repeated MR images. In the other two autopsied patientnts who had MR findings suggestive of cortical laminar necrosis, MR findings were correlated with histological findings. MR imaging was performed with a 1.5-T Magnetom H15 scanner (Siemens, Erlangen, Germany) with a head coil. T1-weighted spin-echo images, with a pulse sequence of 500/15 (repetition time [TR] msec/echo time msec) and long TR spin-echo (2500/15,90) images were obtained in the axial plane, with a 256^<**>256 matrix, a 5-10-mm section thickness, and a field of view of 20-25 cm. Occasionally, additional coronal or sagittal images were obtined. Temporal evolution of MR imaging findings
… More
was arbitrarily divided into frou morphological stages : acute stage, within 1 week after the onset ; early subacute stage, days 11-19 ; late subacute stage, days 21-28 ; and chronic stage, days 41 onward.
Involvement of the watershed zones in the parietooccipitotemporal cortex was most frequent. Cerebral edema was seen in the acute stage. Enhanced T1-weighted images showed cortical laminar enhancement in the early subacute stage ; unenhanced T1-weighted images revealed characteristic laminar hyperintense lesions in the late subacute stage. Both of these findings reflected cortical laminar necrosis at histology. However, we could not elucidate at histological examination what caused the laminar hyperintensity on T1-weighted images. In the chronic stage, cortical atrophy and delayd but progressive white matter changes were seen. Changes in MR imaging features of hypoxic brain damage are complex but distinct. Cortical laminar necrosis and delayd white matter degeneration can be delineated. Less
|
