Levodopa response in Parkinsonism with multiple mitochondrial DNA deletions
Identifieur interne : 001884 ( Istex/Checkpoint ); précédent : 001883; suivant : 001885Levodopa response in Parkinsonism with multiple mitochondrial DNA deletions
Auteurs : Robert A. Wilcox [Australie] ; Andrew Churchyard [Australie] ; Henrik H. Dahl [Australie] ; Wendy M. Hutchison [Australie] ; Denise M. Kirby [Australie] ; Dominic Thyagarajan [Australie]Source :
- Movement Disorders [ 0885-3185 ] ; 2007-05-15.
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Abstract
We report a patient with an autosomal dominant chronic progressive external ophthalmoplegia phenotype associated with multiple mtDNA deletions in muscle from a family in which linkage analysis excluded mutations in DNA polymerase γ (POLG), adenine nucleotide translocase (ANT‐1) or C10orf2 (Twinkle). She presented with prominent Parkinsonism characterized by prolonged benefit from levodopa (L‐dopa) and the later development of L‐dopa induced dyskinesias and motor fluctuations. Thus L‐dopa responsiveness, L‐dopa induced dyskinesias and motor fluctuations may also occur in atypical Parkinsonism of mitochondrial disease, just as they may in multiple system atrophy. © 2007 Movement Disorder Society
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DOI: 10.1002/mds.21416
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<front><div type="abstract" xml:lang="en">We report a patient with an autosomal dominant chronic progressive external ophthalmoplegia phenotype associated with multiple mtDNA deletions in muscle from a family in which linkage analysis excluded mutations in DNA polymerase γ (POLG), adenine nucleotide translocase (ANT‐1) or C10orf2 (Twinkle). She presented with prominent Parkinsonism characterized by prolonged benefit from levodopa (L‐dopa) and the later development of L‐dopa induced dyskinesias and motor fluctuations. Thus L‐dopa responsiveness, L‐dopa induced dyskinesias and motor fluctuations may also occur in atypical Parkinsonism of mitochondrial disease, just as they may in multiple system atrophy. © 2007 Movement Disorder Society</div>
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