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A Case of Cerebellar Dysfunction After Acute Organotin Poisoning
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Ann Occup Environ Med : Annals of Occupational and Environmental Medicine

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HOME > Ann Occup Environ Med > Volume 21(3); 2009 > Article
Case Report A Case of Cerebellar Dysfunction After Acute Organotin Poisoning
Suk Hwan Kim, Cheol In Yoo, Jee Hyun Kwon, Jin Ho Bae, Young Cheol Weon, Yangho Kim

DOI: https://doi.org/10.35371/kjoem.2009.21.3.289
Published online: September 30, 2009
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.
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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.


Ann Occup Environ Med : Annals of Occupational and Environmental Medicine
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