OBJECTIVE: To investigate the nature of parkinsonism associated with liver cirrhosis, which entails examination of the integrity of the nigrostriatal dopaminergic system. METHODS: Consecutive patients who had concurrent liver cirrhosis and parkinsonism were investigated with MRI and dopamine transporter (DAT) single-photon emission computerized tomography (SPECT) using iodine I 123 [(123)I]-radiolabeled fluoropropyl (FP) 2-carbomethoxy-3-(4-iodophenyl) tropane (CIT). RESULTS: Five patients with liver cirrhosis were identified and confirmed to have concurrent parkinsonism. In all patients, MRI showed increased T1 signals, affecting basal ganglia bilaterally. DAT density was normal in four patients, and these patients had relatively non-progressive, levodopa-unresponsive parkinsonism. In one patient, striatal [(123)I]FP-CIT uptake was reduced, similar to the pattern of idiopathic Parkinson's disease (PD). This patient showed sustained response to levodopa treatment. CONCLUSIONS: Our patients showed two different patterns of clinical and neuroradiological features, that is, atypical parkinsonism with normal DAT density, which is clearly differentiated from PD versus levodopa-responsive parkinsonism with reduced DAT density (classical PD). Further investigations using other markers of dopaminergic transmission and histopathological studies should be conducted to elucidate whether damage to the nigrostriatal dopaminergic system occurs in parkinsonism associated with liver cirrhosis. (c) 2010 Elsevier Inc. All rights reserved.
OBJECTIVE: To investigate the nature of parkinsonism associated with liver cirrhosis, which entails examination of the integrity of the nigrostriatal dopaminergic system. METHODS: Consecutive patients who had concurrent liver cirrhosis and parkinsonism were investigated with MRI and dopamine transporter (DAT) single-photon emission computerized tomography (SPECT) using iodine I 123 [(123)I]-radiolabeled fluoropropyl (FP) 2-carbomethoxy-3-(4-iodophenyl) tropane (CIT). RESULTS: Five patients with liver cirrhosis were identified and confirmed to have concurrent parkinsonism. In all patients, MRI showed increased T1 signals, affecting basal ganglia bilaterally. DAT density was normal in four patients, and these patients had relatively non-progressive, levodopa-unresponsive parkinsonism. In one patient, striatal [(123)I]FP-CIT uptake was reduced, similar to the pattern of idiopathic Parkinson's disease (PD). This patient showed sustained response to levodopa treatment. CONCLUSIONS: Our patients showed two different patterns of clinical and neuroradiological features, that is, atypical parkinsonism with normal DAT density, which is clearly differentiated from PD versus levodopa-responsive parkinsonism with reduced DAT density (classical PD). Further investigations using other markers of dopaminergic transmission and histopathological studies should be conducted to elucidate whether damage to the nigrostriatal dopaminergic system occurs in parkinsonism associated with liver cirrhosis. (c) 2010 Elsevier Inc. All rights reserved.