Pretreatment and posttreament positron emission tomographic scan imaging in a 20‐year‐old patient with Wilson's disease
Identifieur interne : 003652 ( Istex/Checkpoint ); précédent : 003651; suivant : 003653Pretreatment and posttreament positron emission tomographic scan imaging in a 20‐year‐old patient with Wilson's disease
Auteurs : Cordato [Australie] ; Michael J. Fulham [Australie] ; Con Yiannikas [Australie]Source :
- Movement Disorders [ 0885-3185 ] ; 1998-01.
English descriptors
Abstract
Wilson's disease is an autosomal‐recessive inherited diorder that results in predominantly hepatic and neurologic manifestations. Neurologic abnormalities include tremor, ataxia, bradykinesia, rigidity, chorea, and dystonia. We report the clinical, radiologic, and serial FDG PET findings in a 20‐year‐old woman who presented with an asymmetric upper limb tremor caused by Wilson's disease. Reduced striatal and cerebral cortical glucose metabolism was demonstrated on a FDG PET study performed before the commencement of D‐penicillamine therapy. After 6 months of treatment, the patient had shown only minimal clinical improvement, despite an increase in striatal and cerebral cortical glucose metabolism on a repeat FDG PET study. After 14 months of treatment, however, a moderate clinical improvement was noted and there was further increase in glucose metabolism on FDG PET.
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DOI: 10.1002/mds.870130131
Affiliations:
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<front><div type="abstract" xml:lang="en">Wilson's disease is an autosomal‐recessive inherited diorder that results in predominantly hepatic and neurologic manifestations. Neurologic abnormalities include tremor, ataxia, bradykinesia, rigidity, chorea, and dystonia. We report the clinical, radiologic, and serial FDG PET findings in a 20‐year‐old woman who presented with an asymmetric upper limb tremor caused by Wilson's disease. Reduced striatal and cerebral cortical glucose metabolism was demonstrated on a FDG PET study performed before the commencement of D‐penicillamine therapy. After 6 months of treatment, the patient had shown only minimal clinical improvement, despite an increase in striatal and cerebral cortical glucose metabolism on a repeat FDG PET study. After 14 months of treatment, however, a moderate clinical improvement was noted and there was further increase in glucose metabolism on FDG PET.</div>
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