- Cyclosporine 신경독성의 뇌 자기공명영상 소견
- ㆍ 저자명
- 양보성
- ㆍ 간행물명
- 대한방사선의학회지
- ㆍ 권/호정보
- 1998년|39권 6호|pp.1049-1056 (8 pages)
- ㆍ 발행정보
- 대한영상의학회
- ㆍ 파일정보
- 정기간행물| PDF텍스트
- ㆍ 주제분야
- 기타
Purpose : To analyze the MR findings of cyclosporine-induced neurotoxicity in patients receiving high dose ofcyclosporine and to suggest the possible pathogenetic mechanism. Materials and Methods : The cases of sevenpatients (2 males, 5 females ; 18-36 years old) who suffered seizures after receiving high-dose cyclosporine forbone marrow transplantation due to diseases such as aplastic anemia or leukemia were retrospectively reviewed. Weevaluated the location and pattern of abnormal signal intensity seen on T2 weighted images, the presence ofcontrast enhancement, and the changes seen on follow-up MR performed at intervals of 12-30 days after initial MRin five of seven patients. We analyzed levels of blood cyclosporine and magnesium, and investigated the presenceof hypertension at the site of the seizure. Results : Locations of the lesions were bilateral(n=5),unilateral(n=2), parietal(n=6), occipital(n=6), temporal(n=4), and in the frontal lobe(n=3). Frontal lesionsshowed high signal intensities in the borderline ischemic zone of the frontal lobe between the territory of theanterior and middle cerebral arteries. In six of the seven patients, cortical and subcortical areas includingsubcortical U-fibers were seen on T2-weighted images to be involved in the parietooccipital lobes. Only one of theseven showed high signal intensity in the left basal ganglia. All lesions showed high signal intensity onT2-weighted images, and iso to low signal intensity on T1-weighted. In five of seven patients there was nodefinite enhancement, but in the other two, enhancement was slight. In four of seven patients seizures occurredwithin high therapeutic ranges (250 - 450 ng/ml), while others suffered such attacks at levels below thetherapeutic range. After cyclospirine was administered at a reduced dosage or stopped, follow-up MR images showedthe complete or near-total disappearance of the abnormal findings previously described. Only two patients hadhypertension, and the others normotension. Five of the seven had hypomagnesemia(1.3 -1.74 mg/dl; N : 1.9 -3.1mg/dl). Conclusion : Most patients with cyclosporine neurotoxicity showed high signal intensity in the corticaland subcortical areas of the parietooccipital lobes, including subcortical U-fiber, as seen on T2 weighted images,and no abnormal enhancement after Gd-DTPA injection. These MR findings should be helpful for the diagnosis ofcyclosporine neurotoxicity.