MR Findings of Cyclosporine Neurotoxicity.
10.3348/jkrs.1998.39.6.1049
- Author:
Po Song YANG
1
;
Kook Jin AHN
;
Bo Young AHN
;
Hae An JUNG
;
Hee Je KIM
;
Jae Mun LEE
Author Information
1. Department of Diagnostic Radiology, St. Mary's Hospital The Catholic University of Korea.
- Publication Type:Original Article
- Keywords:
Drugs, toxicity;
Brain, diseases;
Brain, MR
- MeSH:
Anemia;
Basal Ganglia;
Bone Marrow Transplantation;
Cyclosporine*;
Diagnosis;
Female;
Follow-Up Studies;
Frontal Lobe;
Gadolinium DTPA;
Humans;
Hypertension;
Leukemia;
Magnesium;
Male;
Middle Cerebral Artery;
Plastics;
Retrospective Studies;
Seizures
- From:Journal of the Korean Radiological Society
1998;39(6):1049-1056
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
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 seven patients (2 males, 5 females ; 18-36 years old) who suffered seizures after receiving high-dose cyclosporine for bone marrow transplantation due to diseases such as a plastic anemia or leukemia were retrospectively reviewed. We evaluated the location and pattern of abnormal signal intensity seen on T2 weighted images, the presence of contrast enhancement, and the changes seen on follow-up MR performed at intervals of 12-30 days after initial MR in five of seven patients. We analyzed levels of blood cyclosporine and magnesium, and investigated the presence of 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 lesions showed high signal intensities in the borderline ischemic zone of the frontal lobe between the territory of the anterior and middle cerebral arteries. In six of the seven patients, cortical and subcortical areas including subcortical U-fibers were seen on T2-weighted images to be involved in the parietooccipital lobes. Only one of the seven 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 occurred within high therapeutic ranges (250 - 450 ng/ml), while others suffered such attacks at levels below the therapeutic range. After cyclospirine was administered at a reduced dosage or stopped, follow-up MR images showed the complete or near-total disappearance of the abnormal findings previously described. Only two patients had hypertension, 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 of cyclosporine neurotoxicity.
