A Case of Cerebellar Dysfunction After Acute Organotin Poisoning.
- Author:
Suk Hwan KIM
1
;
Cheol In YOO
;
Jee Hyun KWON
;
Jin Ho BAE
;
Young Cheol WEON
;
Yangho KIM
Author Information
1. Department of Occupational and Environmental Medicine, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan, Korea. yanghokm@nuri.net
- Publication Type:Case Report
- Keywords:
Organotin;
Cerebellar ataxia;
Fluorodeoxyglucose F18
- MeSH:
Adult;
Atrophy;
Brain;
Cerebellar Ataxia;
Cerebellar Diseases;
Fluorodeoxyglucose F18;
Follow-Up Studies;
Humans;
Magnetic Resonance Imaging;
Male;
Neurologic Examination;
Orientation;
Pons
- From:Korean Journal of Occupational and Environmental Medicine
2009;21(3):289-292
- CountryRepublic of Korea
- Language:Korean
-
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.
