Reversible Parkinsonism and T1W pallidal hyperintensities in acute liver failure
Identifieur interne : 002F20 ( Istex/Curation ); précédent : 002F19; suivant : 002F21Reversible Parkinsonism and T1W pallidal hyperintensities in acute liver failure
Auteurs : Annu Aggarwal [Inde] ; Sachin Vaidya [Inde] ; Samir Shah [Inde] ; Joshita Singh [Inde] ; Shrinivas Desai [Inde] ; Mohit Bhatt [Inde]Source :
- Movement Disorders [ 0885-3185 ] ; 2006-11.
English descriptors
Abstract
We report on a young woman who survived acute liver failure (ALF) without liver transplant. During the ALF, she developed a disabling, levodopa‐unresponsive, symmetrical Parkinsonism. This was characterized by severe bradykinesia, mild rigidity, mutism, and prominent gait impairment. Magnetic resonance imaging (MRI) showed bilateral T1W pallidal hyperintensities. Parkinsonism and MRI changes remitted in parallel with normalization of hepatic function. We implicate excessive pallidal manganese deposition secondary to ALF in the pathogenesis of this neuroradiological syndrome. Though hitherto unreported, we propose that Parkinsonism with T1W pallidal hyperintensities may not be uncommon in ALF. © 2006 Movement Disorder Society
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DOI: 10.1002/mds.21096
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<front><div type="abstract" xml:lang="en">We report on a young woman who survived acute liver failure (ALF) without liver transplant. During the ALF, she developed a disabling, levodopa‐unresponsive, symmetrical Parkinsonism. This was characterized by severe bradykinesia, mild rigidity, mutism, and prominent gait impairment. Magnetic resonance imaging (MRI) showed bilateral T1W pallidal hyperintensities. Parkinsonism and MRI changes remitted in parallel with normalization of hepatic function. We implicate excessive pallidal manganese deposition secondary to ALF in the pathogenesis of this neuroradiological syndrome. Though hitherto unreported, we propose that Parkinsonism with T1W pallidal hyperintensities may not be uncommon in ALF. © 2006 Movement Disorder Society</div>
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