• Sichen Li, Yuxia Zhua, and Xi Liu.
• Department of Neurology, the Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
• Med Clin (Barc). 2024 Nov 15; 163 (9): 461468461-468.

AbstractParkinsonism in liver diseases or dysfunction, mainly including neurological manifestations in hereditary liver diseases and neurological complications of advanced liver diseases, occur in isolation or in combination with other movement disorders, and progress along disease course. Prominent akinetic-rigidity syndrome, various onset and progression, poor levodopa response and metabolism abnormalities reflected by serum biomarkers and neuroimaging, make this atypical parkinsonism recognizable and notable in clinical practice. Different susceptibility of brain areas, especially in basal ganglia, to manganese, iron, copper, ammonia overload, together with subsequent oxidative stress, neurotransmitter alterations, disturbed glia-neuron homeostasis and eventually neurotoxicity, contribute to parkinsonism under the circumstances of insufficient liver clearance ability. These mechanisms are interrelated and may interact collectively, adding to the complexity of clinical manifestations and treatment responses. This review summarizes shared clinical features of parkinsonism in liver diseases or dysfunction, depicts their underlying mechanisms and suggests practical flowchart for differential diagnosis.Copyright © 2024. Published by Elsevier España, S.L.U.

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