MRI Findings of Cortical Laminar Necrosis.
10.3348/jkrs.1996.35.5.661
- Author:
Sai Ra YOON
1
;
Jae Chan SHIM
;
Ghi Jae LEE
;
Seong Wook CHOI
;
Su Ok SEONG
;
Myung Jun LEE
;
Ho Kyun KIM
Author Information
1. Department of Diagnostic Radiology, Inje University College of Medicine, Korea.
- Publication Type:Original Article
- Keywords:
Brain, ischemia;
Brain, necrosis;
Brain, MR
- MeSH:
Brain;
Brain Edema;
Female;
Follow-Up Studies;
Frontal Lobe;
Humans;
Hypoxia, Brain;
Magnetic Resonance Imaging*;
Male;
Necrosis*;
Retrospective Studies;
Temporal Lobe
- From:Journal of the Korean Radiological Society
1996;35(5):661-666
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: To evaluate the characteristic sequential MRI findings of cortical laminar necrosis. MATERIALS AND METHODS: We retrospectively reviewed the MRI findings of 11 patients with clinical signs of hypoxic brain damage who showed findings of cortical laminar necrosis with definite time of onset. Three were men and eight were women; they were aged between 27 and 74 (mean 59.3)years. All patients underwent imaging with a 1.0-T MagnetomImpact(Siemens) ; follow-up MR examinations were performed in five. RESULTS: The watershed zones in the parietooccipital, frontoparietal and temporoparietal cortex were involved in eight cases, whereas the other areas involved were the frontal lobe in two cases and the temporal lobe in one. In one case, MRI obtained two days latershowed brain swelling demonstrating obliteration of cortical sulci and high signal intensity of subcortical whitematter on T2WI. In five cases, MRI obtained between two and three weeks later showed gyriform high signalintensity along the cortex on T1WI, cortical high and subcortical low signal intensities on T2WI in four cases,and gyriform enhancement on gadolinium-enhanced scans in three cases. MRI obtained between three and four weeks later in three cases showed subcortical high signal intensity on T2WI in two cases and gyriform cortical highsignal intensities on T1WI and gyral enhancement in all cases. MRI obtained after 50 days in four cases includingtwo of follow-up MR, showed cortical gyriform high signal intensity on T1WI in all cases and subcortical high signal intensity on T2WI and mild gyriform enhancement on gadolinium-enhanced scans in three cases. In twofollow-up studies, the lesions had become more discrete and larger. CONCLUSION: Cortical laminar necrosis due tohypoxic brain damage shows relatively characteristic MR findings according to the stage. Therefore, MR imaging seems to be useful diagnostic tool for the evaluation of cortical laminar necrosis due to hypoxic brain damage.
