Korean J Occup Environ Med.
2009 Sep;21(3):289-292.
A Case of Cerebellar Dysfunction After Acute Organotin Poisoning
- Affiliations
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- 1Department of Occupational and Environmental Medicine, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan, Korea. yanghokm@nuri.net
- 2Department of Neurology and Environmental Medicine, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan, Korea.
- 3Department of Nuclear Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
- 4Department of Radiology, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan, Korea.
Abstract
- BACKGROUND
We performed a follow-up study of an acute organotin poisoning case on the neurological sequelae that remained after 3 years since diagnosis. CASE: In the previous study, a 43-year-old male was reported for acute organotin poisoning. After 3 years, the neurological sequelae were studied using neurological examination, cognitive tests, neurobehavioral tests (by CAYSYS 2000(TM)), brain magnetic resonance imaging (MRI), and 18F-fluorodeoxyglucose (18F-FDG) PET/CT. Upon neurological examination and other tests, orientation was improved compared to that 3 years before, but cerebellar ataxia, dysmetria and dysdiadochokinesia remained the same, with little change. Brain MRI showed cerebellar atrophy. 18F-FDG PET/CT revealed mildly decreased metabolic activity in the pons and in both cerebellar hemispheres. DISCUSSION: This is the first brain MRI study on cerebellar atrophy caused by organotin poisoning. Cerebellar ataxia was confirmed by decreased metabolic activity in 18F-FDG PET/CT.
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